Chapter 9 Inflammation and Immunity BIOL300

01:02:00
https://www.youtube.com/watch?v=1t6EXQO6cr8

摘要

TLDRIn Chapter Nine, the focus is on inflammation and immunity, particularly the mechanisms underlying innate and adaptive immune responses. The innate immune system can recognize and respond to antigens without prior exposure, utilizing mechanisms such as physical barriers (like skin) and cells like neutrophils and macrophages. The adaptive immune system involves B and T lymphocytes, which develop in bone marrow and the thymus, respectively, and respond more efficiently upon second exposure to specific antigens. This chapter highlights the importance of cellular responses, including how immune cells like neutrophils, macrophages, and lymphocytes are derived and function within the body. Additionally, the chapter examines how the complement system, a group of proteins, can enhance the immune response by promoting inflammation and marking pathogens for destruction. Inflammation is described as a protective response that, while essential, can become detrimental if excessive. The signs of inflammation include redness, swelling, heat, pain, and loss of function. Moreover, the differences between active and passive immunity are outlined, with active immunity involving the body's own production of antibodies and passive immunity being obtained through external sources. HIV’s impact on the immune response is discussed, specifically how it targets T-helper cells, which are critical for orchestrating the immune response, impeding the body's ability to fight infections. Vaccines are explained as tools that prime the immune system for a stronger, faster response upon exposure to actual pathogens, exemplifying active immunity.

心得

  • 🛡️ Innate immunity responds to threats without prior exposure.
  • 🔬 Specific defenses include B and T lymphocytes, essential for adaptive immunity.
  • 🦠 Neutrophils and macrophages play key roles in the phagocytic response.
  • 🧬 The complement system enhances inflammatory and immune responses.
  • 🔥 Inflammation is a protective yet potentially harmful bodily response.
  • 🧫 T-helper cells are crucial for coordinating immune responses.
  • 💉 Vaccines prime the immune system for quicker secondary responses.
  • 🦠 HIV impairs immune functions by targeting T-helper cells.
  • 🤧 Antibodies are essential for neutralizing pathogens and toxins.
  • 🌱 Active immunity develops via direct exposure to antigens.
  • 🔄 Passive immunity is obtained through external antibodies.
  • 🧪 Complement cascade aids in attacking foreign cells.

时间轴

  • 00:00:00 - 00:05:00

    The chapter explains the innate immune response which functions without prior exposure to antigens. It includes various cellular defenses like natural killer cells and phagocytic cells, such as neutrophils and macrophages. In contrast, adaptive defenses involving B and T lymphocytes develop upon exposure to antigens and are more selective. The importance of physical barriers like skin and mucosal membranes is discussed, highlighting their antimicrobial molecules like defensins and cryptdins. Disruption of these barriers increases infection risk. The introduction to macrophages is made, emphasizing their role as phagocytes in clearing debris and dead cells and contributing to wound healing.

  • 00:05:00 - 00:10:00

    The lymphatic system's role in immunity is highlighted. It circulates lymph, rich in immune cells, through the body, cleaning debris. The white blood cells, derived from stem cells in red bone marrow, include neutrophils, lymphocytes, monocytes, eosinophils, and basophils, each having distinct roles. Neutrophils are vital for phagocytosis as part of the innate response, whereas lymphocytes distinguish between adaptive and innate responses. Eosinophils handle allergic reactions and parasitic infections, while basophils play a role in inflammation through histamine. Each leukocyte type's abundance in blood is also detailed.

  • 00:10:00 - 00:15:00

    Neutrophils, the most common leukocytes, are crucial in acute bacterial infections, releasing toxins and enzymes for combating pathogens but may also harm healthy tissue. Lymphocytes include T cells, B cells, and natural killer cells. T and B cells function in adaptive immunity responding to specific antigens, while natural killer cells are part of the innate defense. Differences in maturation locations for T and B cells are discussed, highlighting how thymus and bone marrow damage can affect these cells’ development. The division of T cells into helpers and cytotoxic classes is explained, focusing on their roles.

  • 00:15:00 - 00:20:00

    The significance of T helper and cytotoxic T cells in adaptive immunity is explored. T helper cells, with CD4 proteins, activate other immune cells by releasing cytokines, stimulating B cells and macrophages. Cytotoxic T cells with CD8 proteins destroy cells presenting certain antigens, aided by signals from helper T cells. The discussion includes how HIV targets CD4 positive cells, hindering the immune system's capacity to activate and respond robustly. B lymphocytes, with antibody-like receptors, play crucial roles in humoral immunity, producing memory cells for faster future responses and transforming into plasma cells to manufacture antibodies upon activation.

  • 00:20:00 - 00:25:00

    The function of complement proteins in the innate immune response is explained, including their role in inflammation and cell lysis. The formation of the MAC complex by complement activation is detailed, noting its method of lysing cells by creating membrane pores. Chemical mediators like kinins, influencing inflammation and vasodilation, are introduced. The endogenous mechanisms involving Hageman factor in both clotting and inflammation are discussed. Chemotactic cytokines are explained for their role in guiding immune cells to infection sites, illustrating the coordinated effort in innate immunity.

  • 00:25:00 - 00:30:00

    The inflammatory response's purpose of neutralizing threats and facilitating tissue repair is described. Both acute and chronic inflammation are explored, highlighting their characteristics and impacts on tissues, including the potential damage from excessive inflammation. The events of inflammation—vascular permeability increase, leukocyte migration, and phagocytosis—are linked to immune function. Diapedesis and chemotaxis processes enable leukocytes to reach inflamed tissues and contribute to pathogen clearance. The importance of redundant pathways in the immune system is acknowledged for robust defense.

  • 00:30:00 - 00:35:00

    The five cardinal signs of inflammation—redness, swelling, heat, pain, and loss of function—are explained, alongside their contributing factors like vasoactive chemicals and increased vascular permeability. These responses help dilute toxins, enhance immune cell delivery, and initiate healing. However, they can lead to tissue damage if excessive. The content covers inflammatory exudate's role in transporting immune components and facilitating tissue repair. Chemokines and cytokines' roles in immune cell migration and the nuances of leukocyte immigration from blood into tissues are explored in detail.

  • 00:35:00 - 00:40:00

    The process of phagocytosis by immune cells like macrophages and neutrophils involves engulfing pathogens into vesicles called phagosomes, which fuse with lysosomes to destroy the pathogen. Local inflammation symptoms can cause systemic effects such as fever, lethargy, and muscle catabolism. C-reactive protein serves as an indicator of acute inflammation, offering medical professionals a measurable marker. The narrative outlines the differences between innate and adaptive immune responses, emphasizing how memory B cells aid in faster secondary responses to pathogens previously encountered.

  • 00:40:00 - 00:45:00

    Differentiation of self from non-self by B and T cells is achieved through recognition of unique HLA markers, preventing the immune system from attacking self-cells. MHC proteins are categorized into Class I, II, and III, with Class I being crucial for antigen presentation in nucleated cells, while Class II is for phagocytic cells. These systems allow immune cells to recognize viral infections or foreign protein presence. The mechanism by which MHC Class I and II present antigens is described, along with their roles in initiating immune responses via helper T cells and cytotoxic T cells.

  • 00:45:00 - 00:50:00

    The specificity of T cells in recognizing antigens ensures the immune system's precision in targeting threats. Helper T cells activate other immune components, whereas cytotoxic T cells lead to cell lysis of infected cells. The interactions of these cells in HIV pathogenesis are explored, showing how HIV's targeting of CD4 cells disrupts immune signaling. The immune response's sophistication includes memory storage and activation of perforins by cytotoxic T cells to eliminate threats. Memory and effector roles in both B and T cells allow contingency against future infections, with perforins aiding in targeted degradation.

  • 00:50:00 - 00:55:00

    The section covers the types of antibodies, their structures, and functions. Immunoglobulins like IgG, IgM, IgA, IgD, and IgE are explained for their specific roles and occurrence in the body. Antibodies' abilities to neutralize antigens, promote phagocytosis, and activate complements are elaborated. The concept of class-switching in antibody production is discussed for its significance in immune adaptability, and how the presence of specific antibodies can indicate acute or chronic infection is outlined.

  • 00:55:00 - 01:02:00

    The differences between passive and active immunity are explored, emphasizing passive immunity's immediate but temporary benefits, such as maternal antibodies transfer. Active immunity involves the body's development of memory through exposure or vaccination, offering lasting protection. The effectiveness of vaccines in simulating primary immune responses is highlighted, facilitating a quick secondary response upon real pathogen exposure. The importance of maintaining up-to-date vaccinations for effective memory cell activation is stressed, acknowledging limits in absolute immunity but noting enhanced effectiveness of subsequent immune responses.

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思维导图

Mind Map

常见问题

  • What are examples of antigens?

    Antigens can be proteins, glycoproteins, or glycolipids that the immune system recognizes as foreign.

  • How does the innate immune system differ from the specific immune system?

    The innate immune system responds to antigens without prior exposure and non-specifically, while the specific immune system is adaptive, responding more efficiently upon second exposure to specific antigens.

  • What role do neutrophils play in the immune response?

    Neutrophils are part of the innate immune response, acting as phagocytes to engulf foreign debris and microorganisms.

  • How do T and B lymphocytes develop?

    T cells develop in the thymus, while B cells develop in the bone marrow. They become immunocompetent to effectively recognize foreign antigens.

  • What is the function of the complement system?

    The complement system includes plasma proteins that enhance inflammation, lyse target cells, and attract immune cells to sites of infection.

  • What are the five cardinal signs of inflammation?

    The five cardinal signs are redness, swelling, heat, pain, and loss of function.

  • How does HIV affect the immune system?

    HIV targets CD4 positive T-helper cells, impairing the immune system's ability to activate other immune responses.

  • What are the roles of antibodies in the immune system?

    Antibodies neutralize toxins, flag pathogens for destruction, cause agglutination, and activate the complement cascade.

  • What is the difference between active and passive immunity?

    Active immunity involves the body's own antibody production in response to antigens, whereas passive immunity is acquired through external antibodies.

  • What is the role of vaccines in immunity?

    Vaccines stimulate the primary immune response, allowing quicker, stronger secondary responses upon exposure to the actual pathogen.

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  • 00:00:01
    so in this chapter nine uh we're going
  • 00:00:03
    to we're going to talk about
  • 00:00:04
    inflammation and Immunity and we're
  • 00:00:06
    going to first start out here with the
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    innate defenses of immunity uh the
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    innate immune response requires no
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    previous exposure to effectively respond
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    to a given antigen and if you all
  • 00:00:18
    remember from previous classes uh
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    antigens are basically a molecule that
  • 00:00:23
    can stimulate an immune response and
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    these antigens could be things like
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    proteins glycoproteins glycolipids
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    something that the immune system can
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    recognize as being
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    foreign um now the innate defenses
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    include a series of cells like natural
  • 00:00:38
    killer cells which are type of
  • 00:00:39
    lymphocyte and other fosic cells so the
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    cells that can engulf forign debris and
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    microorganisms including neutrophils and
  • 00:00:48
    macras remember the neutrophils are the
  • 00:00:50
    most abundant immune cell um in your
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    white blood cells so then these
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    neutrophils here um are part of your
  • 00:00:59
    inate defense which means your innate
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    defense is pretty widespread so the
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    specific defenses differ than the innate
  • 00:01:06
    defenses because these specific defenses
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    respond more effectively upon second
  • 00:01:12
    exposure to a particular antigen also
  • 00:01:15
    these specific defenses are highly
  • 00:01:17
    selective and can only respond to one
  • 00:01:20
    antigen um one specific type of antigen
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    now these specific defenses involve the
  • 00:01:26
    B and T lymphocytes which we'll go into
  • 00:01:28
    more detail here in a little bit
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    and um this has to be learned so we talk
  • 00:01:33
    about the specific immune defenses as
  • 00:01:36
    being learned or adaptive because they
  • 00:01:39
    uh develop upon exposure to a new
  • 00:01:43
    foreign
  • 00:01:45
    antigen now part of our immune defense
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    relates to different barriers like
  • 00:01:50
    epithelial barriers so it turns out that
  • 00:01:53
    uh even before your immune cells start
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    to fight off Foreign debris or
  • 00:01:57
    microorganisms your skin and mucus
  • 00:01:59
    membranes act as a first line of defense
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    uh for one reason being that the skin
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    epithelium here produces molecules
  • 00:02:07
    called defensin which can basically
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    punch holes in bacterial membranes um
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    and the on top of the fact too that skin
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    is a really tough and protective barrier
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    so that bacteria or other microorganisms
  • 00:02:17
    can't just wiggle through in between
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    your skin cells uh the intestinal
  • 00:02:22
    epithelium you know along your GI tract
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    produces cryptdins which are just a
  • 00:02:27
    class of molecules that again are
  • 00:02:28
    antimicrobial
  • 00:02:30
    now uh disruption of these normal
  • 00:02:32
    epithelial barriers like disruption of
  • 00:02:34
    the skin epithelium or intestinal
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    epithelium can increase the likelihood
  • 00:02:38
    that a pathogen can establish an
  • 00:02:40
    infection so you're more likely to get
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    an infection of skin if there's a wound
  • 00:02:44
    in skin you know where that skin
  • 00:02:46
    epithelium barrier is now compromised or
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    an infection of the gut if there's some
  • 00:02:50
    sort of ulcer or wound within the gut
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    mucosal
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    wall now uh we're going to first talk
  • 00:02:57
    about the macras which are part part of
  • 00:02:59
    your innate immune response uh these
  • 00:03:02
    macroasia are powerful phagocytes and
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    they clean up dead neutrophils and
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    inflammatory debris so they basically
  • 00:03:09
    help remove any dead tissue or dead
  • 00:03:11
    cells and therefore have a role in wound
  • 00:03:14
    healing now macroasia again are part of
  • 00:03:17
    your innate ammun response and so
  • 00:03:20
    they're not specific they can just
  • 00:03:22
    remove a wide variety of antigens in
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    debris and
  • 00:03:27
    microorganisms now most of your immune
  • 00:03:30
    cells are derived from um the lymphoid
  • 00:03:34
    system here and uh it involves a series
  • 00:03:38
    of organs like bone marrow and your
  • 00:03:40
    thymus gland so we know that bone marrow
  • 00:03:42
    especially red bone marrow in particular
  • 00:03:44
    has a variety of stem cells that give
  • 00:03:46
    rise to all of your white blood cells so
  • 00:03:49
    the
  • 00:03:50
    lymphocytes and the rest of your immune
  • 00:03:52
    cells all come from red bone marrow now
  • 00:03:56
    many of these immune cells will develop
  • 00:03:58
    uh in different areas of your body
  • 00:04:00
    including including bone marrow or your
  • 00:04:02
    thymus te- cells in particular develop
  • 00:04:05
    in the thymus and the thymus is a large
  • 00:04:07
    gland it's most active before puberty
  • 00:04:10
    but it's a large gland that sits in the
  • 00:04:12
    medyum just Superior to your heart now
  • 00:04:15
    the lymphocytes are produced from stem
  • 00:04:17
    cells and this includes T and B
  • 00:04:18
    lymphocytes now T lymphocytes migrates
  • 00:04:21
    migrate to the thymus to develop whereas
  • 00:04:23
    B cells and natural killer cells will
  • 00:04:25
    stay in your red bone marrow during
  • 00:04:27
    development and what I mean by
  • 00:04:28
    development is that they need to grow
  • 00:04:31
    and become immunocompetent or basically
  • 00:04:34
    be able to effectively fight infection
  • 00:04:36
    and recognize foreign antigens now there
  • 00:04:40
    are other secondary organs like lymph
  • 00:04:42
    nodes spleen tonsils and Pyers patches
  • 00:04:44
    which you find in your intestin which
  • 00:04:46
    are also involved in immune defense
  • 00:04:48
    because they contain uh high
  • 00:04:50
    concentrations of lymphocytes so you're
  • 00:04:52
    going to find a lot of lymphocytes so TB
  • 00:04:54
    and natural pillar cells in lymph node
  • 00:04:56
    spleen tonsils and pyrus patches so what
  • 00:04:59
    this slide is showing is basically just
  • 00:05:01
    a general overview of your lymphatic
  • 00:05:03
    system and if youall remember from A&P
  • 00:05:05
    the lymphatic system is a series of uh
  • 00:05:08
    vessels that you find in most tissues of
  • 00:05:11
    your body except for bone and teeth but
  • 00:05:13
    these lymph vessels will pick up excess
  • 00:05:16
    fluid from the tissues and then slowly
  • 00:05:18
    carry that excess fluid back towards
  • 00:05:21
    your heart where then the the lymph is
  • 00:05:24
    then mixed back in with your bloodstream
  • 00:05:26
    now what's important to note though with
  • 00:05:27
    respect to the immune system is that
  • 00:05:29
    your lymphoid system is uh basically
  • 00:05:32
    also rich in a lot of lymphocytes or
  • 00:05:34
    immune cells so as that excess fluid
  • 00:05:37
    gets carried back towards your
  • 00:05:38
    bloodstream it's also cleaned up along
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    the way so if there's any debris or
  • 00:05:42
    microorganisms in that fluid uh the
  • 00:05:44
    lymphocytes here in lymph nodes and
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    lymph vessels will help will help clear
  • 00:05:49
    those out um ideally before it goes back
  • 00:05:51
    in your bloodstream and to the rest of
  • 00:05:53
    your body now what this is shown you
  • 00:05:55
    guys are this the the main types of Lucy
  • 00:05:58
    and Lucy are basically just your white
  • 00:06:00
    blood cells now all of these are derived
  • 00:06:02
    from stem cells you find in red bone
  • 00:06:04
    marrow and the major type of Lucy we
  • 00:06:07
    have are the neutrophils lymphocytes
  • 00:06:09
    monocytes eosinophils and the basophils
  • 00:06:13
    now this show this is actually in order
  • 00:06:15
    of their abundance normal abundance in
  • 00:06:18
    the bloodstream so normally you should
  • 00:06:20
    find 60 to 80% of your white blood cells
  • 00:06:23
    are neutrophils 20 to 30% of your white
  • 00:06:25
    blood cells are lymphocytes so B cells T
  • 00:06:28
    cells and natural killer cells include
  • 00:06:31
    the lymphocytes 3 to 8% are monocytes
  • 00:06:34
    which include macrophases uh 1 to 6% are
  • 00:06:37
    eosinophils and then 0 to 2% are
  • 00:06:39
    basophils which are the most are most
  • 00:06:41
    uncommon or least abundant now in terms
  • 00:06:44
    of just the general functions of each of
  • 00:06:46
    these types of Lucy uh the neutrophils
  • 00:06:49
    are first to appear after injury and
  • 00:06:52
    they're involved with phagocytosis
  • 00:06:54
    remember the neutrophils are part of
  • 00:06:56
    your innate immune response so they're
  • 00:06:58
    not specific nor are they adaptive or
  • 00:07:01
    learned they uh more broadly respond to
  • 00:07:05
    a lot of different foreign antigens
  • 00:07:07
    debris or tissue damage and again these
  • 00:07:09
    are the most abundant uh the lymphocytes
  • 00:07:11
    include your B cells and t- cells which
  • 00:07:14
    are part of your learned or adaptive
  • 00:07:16
    immunity or specific immunity and they
  • 00:07:17
    respond to one antigen but the
  • 00:07:19
    lymphocytes also include natural killer
  • 00:07:21
    cells which are part of your innate
  • 00:07:25
    immune
  • 00:07:26
    response now monocytes are a type of
  • 00:07:28
    mobile macras the monocytes are a macras
  • 00:07:32
    or big eater that basically float around
  • 00:07:34
    the bloodstream and they remain in their
  • 00:07:36
    inactive form until they encounter uh
  • 00:07:39
    you know infected tissue or inflammation
  • 00:07:41
    where these monocytes then can activate
  • 00:07:43
    into macras and then enter that infected
  • 00:07:46
    or inflamed tissue and then participate
  • 00:07:48
    in phagocytosis and if you all remember
  • 00:07:50
    from previous slides remember the macras
  • 00:07:52
    are part of your specific I'm not
  • 00:07:56
    specific I'm sorry they're part of your
  • 00:07:57
    innate immune response so the
  • 00:07:59
    eosinophils here uh 1 to 6% of your
  • 00:08:02
    immune cells these are involved in
  • 00:08:04
    allergic reactions and parasitic
  • 00:08:05
    infections and so what's interesting is
  • 00:08:07
    that these are uh potential targets with
  • 00:08:11
    you know allergies and autoimmune
  • 00:08:13
    disease because for whatever reason
  • 00:08:15
    these cells seem to play a role uh if
  • 00:08:18
    they're overactive they seem to play a
  • 00:08:20
    role in you know excessive amounts of
  • 00:08:22
    allergy even even the autoimmune
  • 00:08:24
    response and so there's a there's an
  • 00:08:26
    interesting hypothesis out there that
  • 00:08:28
    talks about how you can use parasites
  • 00:08:31
    possibly to treat Auto autoimmune
  • 00:08:33
    disease and we may come back to that
  • 00:08:35
    later now the basophils uh have a lot of
  • 00:08:39
    histamine granules so they contain a lot
  • 00:08:41
    of histamine now histamine is a type of
  • 00:08:43
    molecule that's released during the
  • 00:08:45
    inflammatory response and during the
  • 00:08:48
    allergy response so basophils are
  • 00:08:51
    important during um inflammation so if
  • 00:08:55
    you inhibit basophils then you inhibit
  • 00:08:57
    the release of histamine and therefore
  • 00:08:59
    reduce things like allergic reactions or
  • 00:09:01
    inflammation and again we'll come back
  • 00:09:03
    to these
  • 00:09:05
    later so we'll first talk about the
  • 00:09:07
    neutrophils here neutrophils remember
  • 00:09:09
    the most abundant of the lucites also
  • 00:09:11
    called the
  • 00:09:12
    polymorphonuclear nucle sites or pmls
  • 00:09:14
    now these are important in acute
  • 00:09:16
    bacterial infections and they release
  • 00:09:18
    toxins like fre rical defensins and
  • 00:09:21
    enzymes such as lasas and although these
  • 00:09:24
    cells normally help to remove dead and
  • 00:09:27
    damaged tissue as well as clar infection
  • 00:09:30
    they can also damage normal tissue so
  • 00:09:32
    excessive nutrifil activities can also
  • 00:09:35
    damage healthy tissue uh near their side
  • 00:09:38
    of activity there there's a little bit
  • 00:09:39
    of um collateral damage there but you
  • 00:09:42
    know it's all it's all in good effort I
  • 00:09:44
    guess now the lymphocytes include
  • 00:09:46
    natural killer cells T cells and B cells
  • 00:09:48
    of these three it's the T and B cells
  • 00:09:51
    that are involved with your specific or
  • 00:09:53
    learned immune response whereas the
  • 00:09:55
    natural killer cells are part of your
  • 00:09:57
    innate immune response so meaning they
  • 00:09:59
    can respond to many different antigens
  • 00:10:01
    and are less specific uh these natural
  • 00:10:04
    killer cells you find in circulation and
  • 00:10:06
    they can migrate from blood into an
  • 00:10:08
    infected tissue when necessary the T
  • 00:10:11
    andb cells are lymphocytes that are part
  • 00:10:14
    of your specific or adaptive immunity
  • 00:10:17
    and they all play different roles in the
  • 00:10:18
    immune response so we'll talk about the
  • 00:10:20
    the specific types of te- cells that are
  • 00:10:22
    involved with immunity as well as the
  • 00:10:24
    specific types of B cells that are
  • 00:10:25
    involved with immunity but what's
  • 00:10:27
    important to note in this slide is that
  • 00:10:29
    T cells mature in the thymus B cells
  • 00:10:31
    mature in bone marrow so if someone has
  • 00:10:34
    damage to the thymus or bone marrow it
  • 00:10:35
    can affect the development of these
  • 00:10:38
    cells now um there are two major classes
  • 00:10:42
    of t-lymphocytes and remember the T
  • 00:10:44
    lymphocytes are part of your specific
  • 00:10:47
    adaptive or learned immune response so
  • 00:10:50
    these two major classes include the t-
  • 00:10:52
    helper and sat toxic tea cells uh it's a
  • 00:10:54
    t- helper cells that are have CD4
  • 00:10:57
    proteins uh these have a function or
  • 00:11:00
    role in activating other te- cells and
  • 00:11:02
    macrophases they can also stimulate B
  • 00:11:05
    cells um by releasing inflammatory cyto
  • 00:11:08
    so when these helper t- cells release
  • 00:11:10
    cyto it can activate B cells to release
  • 00:11:13
    we call antibodies and we'll come back
  • 00:11:15
    to that
  • 00:11:16
    later so think about the te- cells in
  • 00:11:19
    the immune response is it's sort of like
  • 00:11:20
    the cheerleaders of the immune response
  • 00:11:22
    you know they don't participate directly
  • 00:11:24
    in fighting infection rather they can
  • 00:11:27
    release a lot of cyto kindes when they
  • 00:11:31
    recognize infection or tissue damage
  • 00:11:33
    that can activate other immune cells so
  • 00:11:36
    these T helper cells once they release
  • 00:11:38
    cyto they can go on and activate things
  • 00:11:40
    like cytotoxic te- cells or even the B
  • 00:11:43
    cells which we'll talk about soon now
  • 00:11:45
    the cytotoxic te- cells are cd8 positive
  • 00:11:48
    and they do function in killing off uh
  • 00:11:51
    particular cells that contain certain
  • 00:11:54
    antigens however these satox te- cells
  • 00:11:57
    require signals or satchin to be
  • 00:12:00
    released by the t- helper cells in order
  • 00:12:02
    to function normally now the CD4
  • 00:12:05
    proteins and cd8 proteins you find on
  • 00:12:07
    cytotoxic te cells uh these are
  • 00:12:09
    important types of proteins uh involved
  • 00:12:12
    with recognizing foreign antigens but
  • 00:12:14
    what's interesting about these CD4
  • 00:12:16
    proteins is that HIV human imuno
  • 00:12:19
    deficiency virus only infects cells that
  • 00:12:21
    are CD4 positive so specifically it's
  • 00:12:24
    the t- helper cells that are affected
  • 00:12:26
    during the uh HIV infection
  • 00:12:29
    so if HIV infects t- helper cells
  • 00:12:32
    basically what HIV is doing is
  • 00:12:34
    diminishing your immune system's ability
  • 00:12:36
    to get the rest of the immune system
  • 00:12:38
    excited because now there's less t-
  • 00:12:41
    helper cells to release pro-inflammatory
  • 00:12:44
    pyocin which means that other immune
  • 00:12:46
    cells like your cytotoxic tea cells or B
  • 00:12:48
    cells are less responsive to infection
  • 00:12:51
    and that's a sort of Insidious thing
  • 00:12:54
    about uh HIV infection so the B
  • 00:12:57
    lympocytes are also part part of your
  • 00:12:59
    specific adaptive or learned immune
  • 00:13:02
    response and they have antibod like
  • 00:13:04
    receptors on their cell
  • 00:13:05
    surface they carry many copies of
  • 00:13:08
    identical B cell receptors and like the
  • 00:13:10
    t- cells they can only respond to one
  • 00:13:13
    type of antigen now these B cells can
  • 00:13:16
    produce memory cells so once you form a
  • 00:13:18
    certain type of B cell some of the cells
  • 00:13:21
    actually will form clones that actually
  • 00:13:23
    become inactive and they kind of go
  • 00:13:25
    dormant in different areas of your body
  • 00:13:27
    that way you have a learn or a memory of
  • 00:13:30
    the infection if you ever encounter that
  • 00:13:32
    infectious organism again later now many
  • 00:13:35
    of these B lympocytes can survive from
  • 00:13:37
    months to years which is why upon
  • 00:13:39
    subsequent exposure to the same antigen
  • 00:13:42
    your immune system can really respond
  • 00:13:44
    rapidly to that same antigen it's seen
  • 00:13:47
    uh previously now for a typical B cell
  • 00:13:50
    you know we got B cell receptors and
  • 00:13:52
    they can respond to an antigen now
  • 00:13:54
    what's interesting here then is that
  • 00:13:56
    once these B cells recognize a foreign
  • 00:13:58
    antigen their role then is to really
  • 00:14:01
    make antibodies so an activated B cell
  • 00:14:04
    will turn into a clone called a plasma
  • 00:14:07
    cell which is basically just an antibody
  • 00:14:10
    Factory and it starts pumping out
  • 00:14:12
    antibodies to attack uh you know foreign
  • 00:14:15
    antigens now um some other aspects of
  • 00:14:19
    your uh innate immune response include
  • 00:14:22
    what we call complement so complement
  • 00:14:24
    includes 20 different plasma proteins
  • 00:14:26
    which are typically synthesized mostly
  • 00:14:29
    by the liver macroasia and nutrifil and
  • 00:14:33
    these 20 different plasma proteins have
  • 00:14:35
    really important roles in your innate
  • 00:14:37
    immune response so they do things like
  • 00:14:39
    enhance inflammation they can actually
  • 00:14:42
    lice or break apart target cells they
  • 00:14:45
    can actually attract other immune cells
  • 00:14:46
    to a sight of inflammation or infection
  • 00:14:49
    or they can also Target foreign cells
  • 00:14:51
    for removal by um you know immune cells
  • 00:14:55
    so you can see here that once these uh
  • 00:14:58
    complement proteins become activated
  • 00:15:00
    they have these specific functions here
  • 00:15:03
    and so it's important then that you have
  • 00:15:05
    normal liver function macras function
  • 00:15:08
    and nutrifil function to make a
  • 00:15:10
    sufficient amount of complement proteins
  • 00:15:12
    to you know bring this aspect of of the
  • 00:15:16
    immune system
  • 00:15:19
    in now what this is showing are one of
  • 00:15:21
    the complement Cascades and to me this
  • 00:15:23
    is one of the most interesting aspects
  • 00:15:25
    of of compliment where when you have a t
  • 00:15:28
    Target cell and it's maybe recognized as
  • 00:15:30
    being foreign or cancerous what's really
  • 00:15:34
    interesting then is these compliment
  • 00:15:36
    proteins um can activate in response to
  • 00:15:40
    antibodies binding to a foreign antigen
  • 00:15:42
    here once these complement an proteins
  • 00:15:44
    activate they start to arrange in really
  • 00:15:47
    interesting orientation where they form
  • 00:15:50
    this thing called a membrane attack
  • 00:15:52
    complex or MAAC complex and basically
  • 00:15:55
    what this macac complex does is it
  • 00:15:57
    sticks a big old hole in the cell
  • 00:15:59
    membrane of a foreign cell and by having
  • 00:16:02
    a huge hole then in the cell it actually
  • 00:16:04
    causes the cell to rush in with water
  • 00:16:07
    the cell will swell and then burst or
  • 00:16:09
    lice open so basically if a foreign cell
  • 00:16:13
    encounters the complement Cascade it can
  • 00:16:15
    explode because this macac complex
  • 00:16:18
    sticks holes in its membrane and
  • 00:16:20
    therefore allows an excessive amount of
  • 00:16:22
    water to Rush In And this whole cell
  • 00:16:24
    explodes like the Death Star so it's
  • 00:16:27
    actually pretty cool how this uh
  • 00:16:29
    complement Cascade works in the immune
  • 00:16:31
    response now something else that's
  • 00:16:33
    interesting too is that there are
  • 00:16:36
    chemical mediators of immune function
  • 00:16:39
    and these chemical mediators are
  • 00:16:40
    basically a series of chemicals that are
  • 00:16:42
    released by damaged tissue or activated
  • 00:16:45
    immune
  • 00:16:46
    cells and um some of these include the
  • 00:16:48
    kinin um some of the kinin include
  • 00:16:51
    things like Brady kinon or cadin and
  • 00:16:53
    what these chemical mediators do is they
  • 00:16:55
    act in in different ways like they
  • 00:16:57
    promote vasod diil a which can increase
  • 00:17:00
    blood flow to a particular tissue and
  • 00:17:02
    therefore bring in more immune cells
  • 00:17:05
    they can activate inflammation they can
  • 00:17:07
    activate the clotting Cascade they can
  • 00:17:09
    increase vascular permeability which
  • 00:17:11
    does a couple things like dilute it
  • 00:17:13
    dilutes out bacteria and toxins in a
  • 00:17:15
    tissue but it also helps bring in um
  • 00:17:18
    more immune cells to an inflamed or
  • 00:17:20
    infected tissue uh these Canin are also
  • 00:17:23
    involved with smooth muscle contractions
  • 00:17:25
    which help form blood clots and it turns
  • 00:17:27
    out that the kin are also associated
  • 00:17:29
    with pain so if you have an infection or
  • 00:17:33
    inflamed portion of tissue um the pain
  • 00:17:37
    that could be associated with that is
  • 00:17:39
    typically caused by the release of these
  • 00:17:42
    kins now what this is showing is the the
  • 00:17:45
    pathway that leads to the production of
  • 00:17:47
    Kines and what's odd about this pathway
  • 00:17:50
    is that it requires something called
  • 00:17:51
    Haan factor and going back to the
  • 00:17:54
    clotting Cascade you guys remember that
  • 00:17:56
    Haan factor is the common factor
  • 00:17:59
    that's necessary for both the extrinsic
  • 00:18:00
    and intrinsic Pathways of your clotting
  • 00:18:03
    Cascade so what's also interesting then
  • 00:18:05
    is that yes this hement Factor once it's
  • 00:18:07
    activated does promote coagulation of
  • 00:18:10
    blood however it also promotes the
  • 00:18:13
    production of kinin like Brady Kinnon
  • 00:18:15
    that do things like give you a sense of
  • 00:18:17
    pain promote inflammation and also
  • 00:18:20
    promote vasodilation which can increase
  • 00:18:22
    blood flow to an uh an infected or
  • 00:18:25
    inflamed tissue so it turns out that the
  • 00:18:27
    compliment Cascade uh which is involved
  • 00:18:30
    with both
  • 00:18:31
    coagulation as well as the immune system
  • 00:18:34
    also promotes pain inflammation invasive
  • 00:18:37
    dilation now clotting factors do
  • 00:18:40
    function and stop and to stop bleeding
  • 00:18:41
    we talked about that however we just
  • 00:18:43
    learned in the previous slide that
  • 00:18:44
    they're involved with inflammation and
  • 00:18:46
    trigging triggering the kinen system as
  • 00:18:48
    well so there's an interesting interplay
  • 00:18:51
    between all these different systems uh
  • 00:18:53
    of clotting factors as well as uh you
  • 00:18:56
    know inflammation pain and um you know
  • 00:19:00
    coagulation of blood now other chemical
  • 00:19:02
    mediators of your immune function
  • 00:19:04
    include substances like cocin and
  • 00:19:06
    chemokines and these are basic chemicals
  • 00:19:09
    that can act as chemotactic factors now
  • 00:19:13
    chemotaxis literally means chemical
  • 00:19:16
    movement and it's not necessarily the
  • 00:19:18
    movement of those chemicals but rather
  • 00:19:20
    they're chemicals that can attract the
  • 00:19:22
    movement of other immune cells to the
  • 00:19:25
    site of inflammation or infection and so
  • 00:19:28
    what these chemotactic factors can do
  • 00:19:30
    then is enhance and coordinate innate
  • 00:19:33
    and specific immune defenses they can
  • 00:19:35
    activate complex intercellular
  • 00:19:37
    communication networks as well as affect
  • 00:19:40
    the functioning of other nearby
  • 00:19:43
    cells so that these chemotactic factors
  • 00:19:46
    do play an important role in the innate
  • 00:19:48
    defense and inflammation in fact when we
  • 00:19:51
    talk about inflammation it actually is
  • 00:19:52
    part of your innate defense so
  • 00:19:54
    inflammation isn't always a bad thing in
  • 00:19:56
    fact inflammation is part of a normal
  • 00:19:58
    and healthy immune response so there are
  • 00:20:01
    three main purposes to the inflammatory
  • 00:20:03
    response for one it's important for
  • 00:20:05
    inflammation to nutralize and Destroy
  • 00:20:07
    invading and harmful agents inflammation
  • 00:20:10
    also helps to limit the spread of
  • 00:20:11
    harmful agent agents in inflammation
  • 00:20:14
    also sets up the tissue to be repaired
  • 00:20:17
    so these are the three important aspects
  • 00:20:19
    of inflammation but we do know that an
  • 00:20:21
    excessive amount of inflammation can
  • 00:20:24
    lead to uh tissue damage so uh it turns
  • 00:20:28
    out that inflammation occurs with any
  • 00:20:30
    type of cell injury whether it occurs
  • 00:20:32
    exogenously or endogenously an exogenous
  • 00:20:35
    type of cell injury would be like if you
  • 00:20:36
    get a cut and that that directly injures
  • 00:20:39
    injures the tissue otherwise an
  • 00:20:41
    endogenous type of cell injury would be
  • 00:20:42
    like if cells um you know kill
  • 00:20:45
    themselves somehow you know that can
  • 00:20:47
    actually lead to certain types of
  • 00:20:49
    inflammatory responses and really any
  • 00:20:51
    condition that that ends with itis ref
  • 00:20:54
    refers to inflammation so if we talk
  • 00:20:56
    about vasculitis that refers to to
  • 00:20:58
    inflammation of the vasculature or
  • 00:21:00
    appendicitis obviously would be
  • 00:21:02
    inflammation of the appendix so
  • 00:21:04
    inflammation is associated with
  • 00:21:06
    infection but not always you know uh
  • 00:21:08
    sometimes you can just get inflammation
  • 00:21:09
    from tissue damage but not necessarily
  • 00:21:12
    due to infection but infections can
  • 00:21:15
    cause inflammation and we'll we'll
  • 00:21:17
    actually talk about um how those are
  • 00:21:18
    stimulated coming up
  • 00:21:20
    soon now there are five cardinal signs
  • 00:21:23
    of inflammation which include redness
  • 00:21:25
    swelling heat pain and and loss of
  • 00:21:28
    function now the redness we call Emma
  • 00:21:32
    ethema is just sort of a redness of skin
  • 00:21:33
    or tissue that's one of the signs of
  • 00:21:36
    inflammation um what we see that that
  • 00:21:38
    it's also associated with inflammation
  • 00:21:39
    would be swelling or just sort of um
  • 00:21:41
    where the tissue gets sort of in uh
  • 00:21:43
    inflamed or swells with with more fluid
  • 00:21:46
    uh it turns out you guys that uh when
  • 00:21:49
    there's increase in blood flow to a
  • 00:21:50
    particular area you see that inflamed
  • 00:21:53
    tissue gets hotter because there's more
  • 00:21:55
    blood flow there and due to the release
  • 00:21:57
    of kinin you see pain due to tissue
  • 00:21:59
    damage however though these do play
  • 00:22:02
    important roles in those three
  • 00:22:04
    aformentioned functions of inflammation
  • 00:22:07
    so helping to dilute out different
  • 00:22:10
    factors helping to dilute out bacteria
  • 00:22:13
    and also promoting um healing of tissue
  • 00:22:16
    but if these occur in excess it turns
  • 00:22:18
    out that inflammation can lead to loss
  • 00:22:20
    of function or basically tissue damage
  • 00:22:23
    so you know excessive inflammation is
  • 00:22:24
    not a good thing and this is why you
  • 00:22:27
    know if a lot of inflammation in a
  • 00:22:29
    particular part of your body it may be
  • 00:22:30
    important to take some sort of
  • 00:22:32
    anti-inflammatory drug now there's two
  • 00:22:34
    types of inflammation we differentiate
  • 00:22:36
    acute versus chronic and you all
  • 00:22:38
    remember going back to last week we
  • 00:22:39
    talked about how um acute symptoms or
  • 00:22:43
    signs are short in duration but often
  • 00:22:46
    have uh really dramatic initial effects
  • 00:22:51
    uh we Define acute inflammation is
  • 00:22:53
    lasting less than two weeks and it often
  • 00:22:55
    involves a discrete set of in events
  • 00:22:57
    events like getting cut and then being
  • 00:22:59
    acutely inflamed due to that cut or
  • 00:23:03
    burn however chronic inflammation
  • 00:23:05
    differs from acute inflammation because
  • 00:23:07
    it's more diffuse it's kind of more
  • 00:23:08
    widespread throughout your body extends
  • 00:23:10
    over longer periods of time right more
  • 00:23:12
    than two weeks it can result in Scar
  • 00:23:14
    Tissue formation or deformity of that
  • 00:23:16
    tissue it can also lead to granuloma
  • 00:23:18
    formation which is basically kind of
  • 00:23:20
    like a hardness of the tissue so you get
  • 00:23:23
    a little bit of loss of function of
  • 00:23:24
    there as well so in in many cases
  • 00:23:27
    chronic inflammation
  • 00:23:28
    can be um you know more dramatic or at
  • 00:23:32
    least damaging to tissues versus acute
  • 00:23:35
    inflammation now there are three major
  • 00:23:37
    events that occur uh with the initial
  • 00:23:40
    inflammatory response for one we see an
  • 00:23:43
    increase in vascular permeability due to
  • 00:23:46
    the fact that mass cells uh release
  • 00:23:49
    vasoactive chemicals uh you find these
  • 00:23:51
    mass cells in tissue and they basically
  • 00:23:54
    just kind of monitor um whether there
  • 00:23:56
    are uh you know am uh infectious
  • 00:24:00
    microorganisms nearby or if there's any
  • 00:24:02
    tissue damage if if either occurs
  • 00:24:05
    they'll release vasoactive chemicals
  • 00:24:06
    like histamine prostaglandins and lucrin
  • 00:24:09
    which increase vascular permeability
  • 00:24:12
    what this means is that blood vessels
  • 00:24:13
    become more permeable or more leaky so
  • 00:24:16
    that some of the components in blood
  • 00:24:17
    like water or compliment proteins can
  • 00:24:20
    start to leak out in the tissue causing
  • 00:24:23
    things like inflammation or
  • 00:24:26
    swelling as well as uh bringing
  • 00:24:28
    complement proteins that can Aid in the
  • 00:24:31
    process of the immune response now uh
  • 00:24:33
    another event that occurs during
  • 00:24:35
    inflammation is the immigration of Lucy
  • 00:24:38
    what we find then is that due to the
  • 00:24:40
    release of vasoactive chemicals uh this
  • 00:24:43
    can attract Lucy through chemotaxis so
  • 00:24:46
    that white blood cells in the
  • 00:24:48
    bloodstream can start to marginate or
  • 00:24:51
    basically move through the blood vessel
  • 00:24:53
    wall from blood into the tissue it turns
  • 00:24:56
    out these actually will move through a
  • 00:24:58
    process called diapedesis where they
  • 00:24:59
    kind of squeeze between cells and this
  • 00:25:01
    is attracted through chemotaxis where
  • 00:25:04
    these glucosides lucites can kind of
  • 00:25:06
    sniff out or smell uh these chemical
  • 00:25:10
    markers of inflammation and they're
  • 00:25:12
    attracted those markers therefore can
  • 00:25:14
    leave blood and enter that inflamed
  • 00:25:16
    tissue now the third event in
  • 00:25:18
    inflammation is fagocitosis where we
  • 00:25:20
    have neutrophils and macrophases
  • 00:25:22
    remember this is part of your um your
  • 00:25:25
    innate immune response these produce PR
  • 00:25:27
    proteolytic enzymes and oxid oxidizing
  • 00:25:30
    agents that help to break down the
  • 00:25:33
    phagocytose or digested material and
  • 00:25:36
    therefore start to remove any foreign
  • 00:25:39
    microorganisms or dead tissue um away
  • 00:25:42
    from a local
  • 00:25:43
    area now these three events of
  • 00:25:45
    inflammation can see here so uh what
  • 00:25:47
    happens you guys with with inflammation
  • 00:25:49
    you get some sort of tissue injury and
  • 00:25:51
    we talked about that with tissue injury
  • 00:25:53
    that leads to the the release of
  • 00:25:55
    vasoactive chemicals that can lead to
  • 00:25:57
    things like vasod dilation uh vasod
  • 00:26:00
    dilation will increase blood flow to
  • 00:26:01
    that tissue which allows for more white
  • 00:26:03
    blood cells to enter that inflamed
  • 00:26:05
    tissue and therefore participate in the
  • 00:26:08
    fosic immune response otherwise injury
  • 00:26:11
    can also lead to the release of
  • 00:26:12
    chemokines that can also promote
  • 00:26:14
    phagocytosis as well as uh nutrifil and
  • 00:26:17
    macro macras is leaving or marginating
  • 00:26:20
    from the from the bloodstream and
  • 00:26:22
    entering uh that infected tissue to also
  • 00:26:25
    participate in phagocytosis so you can
  • 00:26:28
    see here then that there are multiple
  • 00:26:31
    Pathways that result from injury that
  • 00:26:33
    all lead to phagocytosis or basically uh
  • 00:26:37
    engulfing of that debris or or
  • 00:26:39
    microorganisms that can that can Aid or
  • 00:26:41
    participate in the immune response and
  • 00:26:44
    you might wonder you know well why do
  • 00:26:45
    you have three different Pathways that
  • 00:26:47
    do the same thing well you know we know
  • 00:26:49
    that immune system or
  • 00:26:51
    fyos is such an important thing that
  • 00:26:54
    you'd want some redundancy here you want
  • 00:26:56
    some backup plans where let's say if one
  • 00:26:58
    fails at least you have other mechanisms
  • 00:27:00
    that can promote the same
  • 00:27:03
    process now remember this show the we
  • 00:27:06
    have the five cardinal signs of
  • 00:27:07
    inflammation which include pain heat
  • 00:27:09
    redness and swelling and what this slide
  • 00:27:12
    is showing are the different factors
  • 00:27:13
    that lead to each of those uh cardinal
  • 00:27:16
    signs and actually one of the signs
  • 00:27:17
    that's missing up here because there's
  • 00:27:18
    only four here is the loss of function
  • 00:27:21
    so if you get too much pain heat redness
  • 00:27:23
    and swelling that can lead to loss of
  • 00:27:25
    function but uh the pain the heat the
  • 00:27:28
    renis and swelling are important aspects
  • 00:27:31
    of the inflammatory immune response so
  • 00:27:34
    what happens then is that with tissue
  • 00:27:36
    damage we we get the release of
  • 00:27:37
    vasoactive and chemotactic factors and
  • 00:27:40
    these do a variety of things for one we
  • 00:27:43
    know that vasoactive chemicals and
  • 00:27:45
    chemotactic factors can lead to the
  • 00:27:47
    production of pain um through the kinan
  • 00:27:50
    pathway so that you you know you can get
  • 00:27:53
    some pain um due to the release of these
  • 00:27:55
    chemicals it turns out that Vaso active
  • 00:27:57
    chemicals can also promotee vasodilation
  • 00:28:00
    and this vasod dilation can increase
  • 00:28:02
    blood flow which actually will cause
  • 00:28:05
    redness heat and too much blood flow
  • 00:28:08
    also can lead to some pain due to
  • 00:28:11
    swelling uh in that tissue um these
  • 00:28:14
    chemotactic and vasoactive factors can
  • 00:28:16
    also increase the permeability of your
  • 00:28:18
    of your blood vessels which cause
  • 00:28:20
    swelling in a local area and that
  • 00:28:22
    swelling uh is involved in helping to
  • 00:28:24
    dilute out any toxins dilute out the
  • 00:28:27
    bacteria and also help bring in some of
  • 00:28:30
    the nutrients and complement proteins
  • 00:28:33
    that Aid in the process of the immune
  • 00:28:36
    response here and last but not least you
  • 00:28:38
    guys that the vasoactive and Cho
  • 00:28:40
    chemotactic factors also promote the
  • 00:28:44
    immigration of neutrophils from your
  • 00:28:45
    bloodstream into that tissue which also
  • 00:28:49
    release a series of factors that promote
  • 00:28:51
    swelling now too much pain heat and
  • 00:28:53
    swelling and redness uh can lead to loss
  • 00:28:56
    of function which um can damage tissue
  • 00:28:59
    so again you know inflammation is part
  • 00:29:01
    an is an important part of your immune
  • 00:29:03
    response however too much inflammation
  • 00:29:06
    um can lead to damage of your body's
  • 00:29:11
    tissues so the fluid that is actually
  • 00:29:14
    going to be um coming from the increased
  • 00:29:17
    vascular permeability we call
  • 00:29:19
    inflammatory exate so the inflammatory
  • 00:29:22
    exit dates are due to the transport of
  • 00:29:24
    Lucy and antibodies um so this basically
  • 00:29:28
    allows for these substances to come from
  • 00:29:30
    blood into the tissue um it's also
  • 00:29:32
    involved with diluting toxins and
  • 00:29:34
    irrigating substances as well as
  • 00:29:36
    transportation of nutrients into the
  • 00:29:38
    inflamed tissue for its repair so
  • 00:29:42
    exitation inflammatory exate is
  • 00:29:44
    basically just the fluid that leaks from
  • 00:29:46
    those in those uh permeable vessels
  • 00:29:49
    remember the it's the chemotactic and
  • 00:29:51
    sakin that really that increase the uh
  • 00:29:53
    permeability of blood vessels so what is
  • 00:29:56
    what is uh immigration and margination
  • 00:29:59
    look like well it turns out that once
  • 00:30:01
    these satchin are released by activated
  • 00:30:06
    macrophases um they're going to travel
  • 00:30:07
    on over to the blood vessel wall here
  • 00:30:11
    and once they travel to the blood vessel
  • 00:30:13
    wall uh they can activate a series of
  • 00:30:16
    receptors that then allow for lucco
  • 00:30:19
    sites then to roll across the blood
  • 00:30:22
    vessel wall stick to that activated
  • 00:30:25
    receptor with the chemokine
  • 00:30:27
    once this blood cell cell is stuck to
  • 00:30:29
    the blood vessel wall it can start to
  • 00:30:32
    squeeze its way through or marginate
  • 00:30:34
    through in between two cells and then
  • 00:30:38
    enter the infected or inflamed tissue um
  • 00:30:41
    once in the infected or inflamed tissue
  • 00:30:43
    you know it'll attach to the
  • 00:30:44
    extracellular Matrix within that tissue
  • 00:30:46
    and then allow basically walk around the
  • 00:30:49
    tissue and and find any microorganisms
  • 00:30:52
    or um dead cells to
  • 00:30:56
    remove now now the process of
  • 00:30:58
    Phagocytosis which we talked about was
  • 00:31:00
    mediated by things like macroasia and
  • 00:31:03
    nutrifil is kind of an interesting and
  • 00:31:06
    uh can be a complex process but what
  • 00:31:09
    happens is let's say if the immune cell
  • 00:31:12
    here uh phagocytosis a microb well what
  • 00:31:16
    that what happens then is it puts it
  • 00:31:18
    into what we call a
  • 00:31:19
    fome which is basically just a vesicle
  • 00:31:22
    that results from phagocytosis that
  • 00:31:24
    contains your microb within it and then
  • 00:31:27
    what happens is the immune cell like a
  • 00:31:29
    neutrophil or macras will fuse lomes
  • 00:31:33
    with this fome to form what we call a
  • 00:31:35
    fago liome now remember lomes are full
  • 00:31:38
    of lots of different enzymes and acid
  • 00:31:41
    that can act to basically uh break down
  • 00:31:44
    this foreign microbe here and it can do
  • 00:31:47
    this through a process of like
  • 00:31:49
    antioxidants or enzymes and even acid
  • 00:31:52
    that basically break down the chemical
  • 00:31:54
    structure of the uh basically the microb
  • 00:31:58
    inside of this Falone once the microb is
  • 00:32:00
    broken down then you know the cell can
  • 00:32:02
    recycle those
  • 00:32:04
    components and that's how these microbes
  • 00:32:07
    are removed from your
  • 00:32:08
    body now there are some systemic
  • 00:32:11
    manifestations of inflammation we know
  • 00:32:14
    that the local inflamm signs of symptoms
  • 00:32:17
    of inflammation include those five
  • 00:32:19
    cardinal signs we talked about so the
  • 00:32:21
    redness heat the pain the swelling and
  • 00:32:23
    the loss of function which are
  • 00:32:25
    associated with both acute and chronic
  • 00:32:27
    inflammation however local inflammation
  • 00:32:30
    can lead to systemic involvement because
  • 00:32:33
    some of the inflammatory molecules that
  • 00:32:35
    are released B inflamed tissue can make
  • 00:32:38
    it into your bloodstream uh once they go
  • 00:32:40
    systemic these inflammatory molecules
  • 00:32:42
    can do things like induce Fever by
  • 00:32:45
    basically resetting your hypothalamus to
  • 00:32:47
    run your body temperature a little
  • 00:32:49
    higher than normal uh can also uh
  • 00:32:52
    increase the production of
  • 00:32:54
    neutrophils um and cause you to feel
  • 00:32:57
    feel more lethargic and it can also
  • 00:32:59
    increase muscle catabolism so remember
  • 00:33:01
    catabolism means to breakdown so your
  • 00:33:03
    body can start to use uh protein and
  • 00:33:06
    muscle for
  • 00:33:08
    energy now one of the markers of acute
  • 00:33:12
    uh inflammation is called C reactive
  • 00:33:14
    protein and so C reactive protein is one
  • 00:33:16
    of those blood markers for acute
  • 00:33:20
    inflammation and we can also measure how
  • 00:33:23
    much inflammation someone has in their
  • 00:33:24
    body in a laboratory setting by
  • 00:33:26
    measuring their arthrite sedimentation
  • 00:33:28
    rate or ESR and if their ESR um is
  • 00:33:32
    higher this will increase with
  • 00:33:36
    inflammation now the specific immune
  • 00:33:39
    system uh is remember part of your
  • 00:33:42
    immune system that can respond to a
  • 00:33:44
    specific antigen now although when we
  • 00:33:47
    just talked about the inflammatory
  • 00:33:49
    response that was part of your innate uh
  • 00:33:52
    immune response the specific adaptive
  • 00:33:54
    immune response could be activated as
  • 00:33:56
    well as well if those microbes hung
  • 00:33:59
    around the tissue long enough to be
  • 00:34:01
    recognized by a B cell or a t- cell so
  • 00:34:04
    these B cells and te- cells which are
  • 00:34:06
    part of your specific adaptive immunity
  • 00:34:08
    recognize foreign Invaders and they act
  • 00:34:10
    to destroy those foreign Invaders what's
  • 00:34:13
    also interesting too is they can retain
  • 00:34:14
    a memory of that encounter that way if
  • 00:34:17
    you're subsequently exposed to those
  • 00:34:19
    foreign Invaders um this going to is
  • 00:34:22
    going to allow for a more effective and
  • 00:34:24
    quick uh secondary immune response the
  • 00:34:26
    next time you're exposed to that
  • 00:34:28
    microorganism so the main cell types
  • 00:34:30
    that are involved with a specific
  • 00:34:31
    adaptive immune response are your B
  • 00:34:33
    cells and t- cells uh B cells are
  • 00:34:35
    involved with humoral immunity the
  • 00:34:37
    reason why we call it humoral immunity
  • 00:34:38
    is that the humors of your body or body
  • 00:34:41
    fluids and B cells release antibodies
  • 00:34:44
    into your body fluids to basically find
  • 00:34:47
    and attach to foreign microbes or
  • 00:34:50
    antigens now te- cells we call cell
  • 00:34:53
    mediated immunity because the te- cells
  • 00:34:56
    are involved involved with specifically
  • 00:34:59
    targeting um foreign cells now one of
  • 00:35:02
    the challenges that B cells and T cells
  • 00:35:05
    must undergo is differentiating self
  • 00:35:09
    from non-self you know how do B cells
  • 00:35:11
    and T cells recognize that a that a cell
  • 00:35:14
    belongs in your body so we call it a
  • 00:35:16
    self cell or how does it recognize that
  • 00:35:18
    a cell is foreign or
  • 00:35:21
    non-self now it does this through what
  • 00:35:23
    we call the major histo compatibility
  • 00:35:25
    complex um also called the human Lucy
  • 00:35:28
    antigen or
  • 00:35:30
    HLA each individual person has their own
  • 00:35:34
    HLA markers that Mark their own body's
  • 00:35:37
    cells as self it turns out that your
  • 00:35:40
    your individual and unique HLA markers
  • 00:35:44
    are dependent on your genotype and last
  • 00:35:47
    week we talked about how
  • 00:35:49
    [Music]
  • 00:35:51
    genotype you know inheritance patterns
  • 00:35:54
    that kind of stuff so everyone on the
  • 00:35:56
    planet it unless they identical twins
  • 00:35:58
    has their own um unique HLA which
  • 00:36:02
    basically marks their body cells as self
  • 00:36:06
    now no one has the same image see unless
  • 00:36:08
    they're identical twins and this is
  • 00:36:10
    because of uh genetic recombination
  • 00:36:12
    which occurs during meiosis we get sort
  • 00:36:15
    of shuffling of genes and so even for
  • 00:36:17
    close relatives like brothers and
  • 00:36:19
    sisters which you know presumably have
  • 00:36:21
    the same genes the thing is though is
  • 00:36:24
    that they inherit different combinations
  • 00:36:26
    of the types of those genes or forms of
  • 00:36:28
    those genes from their parents due to
  • 00:36:30
    shuffling of genes during meiosis so
  • 00:36:33
    even if you have a brother and sister um
  • 00:36:36
    that you inherit your DNA from the same
  • 00:36:37
    parents you have different forms of
  • 00:36:40
    those genes from each parent which means
  • 00:36:42
    you're even though you're interrelated
  • 00:36:44
    you're also slightly different now MHC
  • 00:36:48
    comes from basically your genome so your
  • 00:36:52
    chromosomes and there's different
  • 00:36:53
    classes of MHC we have class one two and
  • 00:36:55
    three class 1 MHC are basically
  • 00:36:59
    receptors for antigen presentation for
  • 00:37:02
    nucleated cells Class 2 MHC are
  • 00:37:05
    receptors for antigen presentation found
  • 00:37:07
    on macras and B cells and class 3 MHC
  • 00:37:12
    are used for complement components and
  • 00:37:15
    other immune
  • 00:37:16
    cells now uh nucleated cells all Express
  • 00:37:20
    MHC class one receptors on their cell
  • 00:37:23
    surface and this is important because
  • 00:37:25
    cytotoxic cells can recognize these
  • 00:37:27
    antigens um on mhcu class one cells and
  • 00:37:31
    then recognize whether those cells are
  • 00:37:33
    foreign or they belong in your cell
  • 00:37:36
    other specialized cells like dendritic
  • 00:37:38
    cells macrophases B cells Express MHC
  • 00:37:41
    Class 2 proteins and these uh play a
  • 00:37:44
    role with the t- helper cells in
  • 00:37:46
    recognizing antigens as being foreign or
  • 00:37:50
    belonging to
  • 00:37:51
    yourself now it turns out that nucleated
  • 00:37:54
    cells are continuously producing mhc1
  • 00:37:57
    proteins by their endoplasmic reticulum
  • 00:38:00
    and it turns out that as these are
  • 00:38:02
    producing MHC class one proteins these
  • 00:38:05
    actually will fuse with other protein
  • 00:38:07
    fragments in the cytoplasm so what's
  • 00:38:09
    kind of odd is that these MHC class one
  • 00:38:12
    proteins are used as a marker to kind of
  • 00:38:16
    identify what's going on inside of cells
  • 00:38:18
    because they're constantly binding with
  • 00:38:20
    little fragments within those cells now
  • 00:38:22
    what happens is these MHC class 1
  • 00:38:24
    proteins and those peptide frag
  • 00:38:26
    fragments eventually get expressed on
  • 00:38:29
    the cell surface and these are expected
  • 00:38:31
    by T I'm sorry these are inspected by
  • 00:38:34
    the T
  • 00:38:36
    cells around the humor or fluids of your
  • 00:38:40
    body now what's interesting here then is
  • 00:38:42
    that these te cells then by recognizing
  • 00:38:45
    mhc1 complexes uh with the peptide
  • 00:38:49
    fragments can really kind of see what's
  • 00:38:51
    going on inside of your body cells uh in
  • 00:38:54
    real time so so the reason why this is
  • 00:38:57
    important is that this is one of the
  • 00:38:59
    ways that cytotoxic tea cells can
  • 00:39:01
    recognize whether a cell is virally
  • 00:39:03
    infected or not you know because we know
  • 00:39:06
    that viruses must get inside of a cell
  • 00:39:09
    in order to divide so how do we know
  • 00:39:11
    whether our immune cells know if a a
  • 00:39:15
    cell contains a virus or doesn't contain
  • 00:39:17
    a virus well once that virus enters a
  • 00:39:20
    cell you know it takes its genome and
  • 00:39:23
    starts to use the host cell Machinery to
  • 00:39:25
    make viral proteins now it turns out
  • 00:39:28
    those viral proteins will fuse with a
  • 00:39:30
    class one MHC receptor which then gets
  • 00:39:33
    expressed on the cell surface so
  • 00:39:35
    basically it's a way for the cell to
  • 00:39:37
    show hey it has viral proteins inside of
  • 00:39:40
    it and this is one of the ways that the
  • 00:39:42
    cytotoxic tea cells can recognize
  • 00:39:45
    whether there are viral proteins being
  • 00:39:47
    expressed in a given cell of your body
  • 00:39:49
    if this is the case if a cot toxic te-
  • 00:39:51
    cell recognizes that a cell is virally
  • 00:39:54
    infected this cot toxic t cell then will
  • 00:39:57
    initiate um the process of
  • 00:40:01
    uh basically coordinated cell death
  • 00:40:04
    which is apotosis so cytotoxic te cells
  • 00:40:06
    will then kill a virally infected cell
  • 00:40:09
    which is kind of interesting now this
  • 00:40:11
    differs from the class 2 MHC proteins
  • 00:40:14
    because MH Class 2 MHC proteins present
  • 00:40:17
    antigens that are obtained from the
  • 00:40:19
    extracellular sources remember this
  • 00:40:22
    differs from class one MHC because class
  • 00:40:24
    one actually obtains proteins from
  • 00:40:26
    within cells class two obtains proteins
  • 00:40:29
    that you find outside of cells so that
  • 00:40:32
    these ones are associated with the the
  • 00:40:34
    phagocytic cells like neutrophils and
  • 00:40:38
    macras now it turns out these
  • 00:40:40
    extracellular antigens or proteins must
  • 00:40:43
    first be ingested by antigen presenting
  • 00:40:45
    cells like macroasia and nutrifil
  • 00:40:48
    through a process of
  • 00:40:49
    Phagocytosis so that these
  • 00:40:52
    um macras and nutrifil will fake oyos
  • 00:40:57
    any kind of extracellular debris it'll
  • 00:41:00
    basically fuse that with lome and chop
  • 00:41:02
    this up into little bits it can take
  • 00:41:04
    those peptide fragments fuse it with a
  • 00:41:06
    Class 2 MHC receptor and then Express
  • 00:41:09
    that on its cell surface this is one of
  • 00:41:11
    the ways that these cells can present
  • 00:41:13
    antigens to other immune cells to get
  • 00:41:16
    the rest of the immune cell excited um
  • 00:41:18
    in some ways it's kind of basically kind
  • 00:41:20
    of showing what it caught so once it
  • 00:41:23
    catches this foreign protein it'll chop
  • 00:41:25
    it up put it on mhc2 MHC Class 2
  • 00:41:28
    receptor exess Express that on its cell
  • 00:41:31
    surface and then say hey helper T cell
  • 00:41:33
    look what I found and then the helper T
  • 00:41:35
    cell will will recognize this as being
  • 00:41:37
    foreign and then that will help initiate
  • 00:41:40
    an immune response because if you
  • 00:41:41
    remember helper T cells release cokin
  • 00:41:44
    which then can then can activate the
  • 00:41:46
    cytotoxic te- cells and your B
  • 00:41:50
    cells so um uh it turns out that cell
  • 00:41:55
    mediated immunity involves your te-
  • 00:41:57
    cells and uh these te- cells have their
  • 00:42:00
    own specific receptors and it's used to
  • 00:42:03
    recognize foreign antigens that you find
  • 00:42:05
    on antigen presenting cells now these
  • 00:42:08
    te- cells are specific so they only
  • 00:42:10
    recognize one specific type of antigen
  • 00:42:14
    but what this means then is that you
  • 00:42:15
    have lots of different types of te-
  • 00:42:17
    cells that respond to their own specific
  • 00:42:20
    type of antigen and what this allows for
  • 00:42:23
    then is your immune system can recognize
  • 00:42:25
    potentially Millions or billions of
  • 00:42:27
    different types of antigens uh which may
  • 00:42:30
    be foreign to your body and we know that
  • 00:42:32
    there's two types of te- cells we have
  • 00:42:33
    the helper and cytotoxic te- cells and
  • 00:42:35
    the function of these helper te- cells
  • 00:42:37
    which are CD4 positive is to release
  • 00:42:40
    cines that activate other immune cells
  • 00:42:42
    and the cytotoxic te- cells are the ones
  • 00:42:45
    that directly participate in the immune
  • 00:42:47
    response by basically you know directly
  • 00:42:50
    targeting a foreign cell so the T cells
  • 00:42:53
    we talked about with CD4 positive you
  • 00:42:54
    know these are involved with with the
  • 00:42:56
    MHC Class 2 pathway they're CD4 positive
  • 00:42:59
    so that they're going to be possibly
  • 00:43:01
    infected by the HIV virus and um these
  • 00:43:05
    recognize one specific type of antigen
  • 00:43:08
    and this differs from cytotoxic te-
  • 00:43:10
    cells because these are cd8 positive um
  • 00:43:12
    these are involved with the MHC class
  • 00:43:14
    one pathway um now HIV does not infect
  • 00:43:18
    cd8 positive cells but HIV still has an
  • 00:43:22
    a dramatic effect on your immune system
  • 00:43:24
    because you're removing the CD4 positive
  • 00:43:28
    uh set helper T cells which are
  • 00:43:30
    necessary to get the rest of your immune
  • 00:43:31
    system
  • 00:43:33
    excited now uh once these um cd8
  • 00:43:38
    proteins um are used with this mhc1
  • 00:43:42
    pathway it can trigger a response that
  • 00:43:45
    causes cytotoxic tea cells um to
  • 00:43:49
    activate also other cells like t- helper
  • 00:43:52
    cells and so uh it turns out that it's
  • 00:43:55
    not enough that you only have cot toxic
  • 00:43:58
    te- cells recognizing something foreign
  • 00:44:00
    it also requires unique co- stimulation
  • 00:44:03
    by Inner lucans and cocin released by
  • 00:44:06
    the helper te- cells so it's almost as
  • 00:44:08
    though these cytotoxic te- cells need
  • 00:44:10
    other immune cells to kind of
  • 00:44:12
    corroborate its story that it's
  • 00:44:14
    recognizing a foreign
  • 00:44:17
    microorganism now the cytotoxic te-
  • 00:44:19
    cells um once activated can proliferate
  • 00:44:22
    into memory cells and affector cells the
  • 00:44:25
    memory cells will remain dormant and
  • 00:44:27
    store a memory of that infection whereas
  • 00:44:29
    the affector cells are the ones that are
  • 00:44:31
    the will participate directly in the
  • 00:44:34
    immune response by targeting that
  • 00:44:36
    foreign microorganism and the way that
  • 00:44:39
    these cot toxic tea cells remove foreign
  • 00:44:41
    microorganisms these affector cells do
  • 00:44:43
    is that they produce something called
  • 00:44:44
    perforins and these perforins are
  • 00:44:46
    manufactured by cytotoxic tea cells and
  • 00:44:49
    they basically um punch holes instead of
  • 00:44:52
    foreign cells and then inject granzymes
  • 00:44:55
    into the Target cell which degrades its
  • 00:44:57
    DNA and allows for apotosis or basically
  • 00:45:00
    cell death to
  • 00:45:02
    occur so I like to think about these cot
  • 00:45:04
    toxic tea cells as being like the grim
  • 00:45:06
    reapers of your immune system because
  • 00:45:08
    once they touch a foreign
  • 00:45:10
    microorganism or uh you know like a
  • 00:45:13
    cancer cell it can actually cause that
  • 00:45:15
    cell to kill itself through a process of
  • 00:45:17
    apotosis which is actually pretty cool
  • 00:45:20
    now the B cells are involved with your
  • 00:45:22
    humoral immunity and there's two major
  • 00:45:24
    types of B cells we have memory cells
  • 00:45:26
    and plasma cells so once B cells are
  • 00:45:28
    activated you know some of these cells
  • 00:45:30
    will go dormant and store a memory of
  • 00:45:31
    that infection that way your immune
  • 00:45:33
    system is ready to uh remember that
  • 00:45:36
    infection in the future otherwise the
  • 00:45:38
    plasma cells are the activated B cells
  • 00:45:41
    that are basically like big old antibody
  • 00:45:44
    factories and um once these cells are
  • 00:45:47
    activated um they divide into clones so
  • 00:45:49
    you can get a lot of different plasma
  • 00:45:51
    cells that can really rapidly produce a
  • 00:45:54
    lot of antibodies
  • 00:45:56
    now these antibodies are basically short
  • 00:45:59
    I'm sorry the plasma cells are
  • 00:46:00
    short-lived antibod producing factories
  • 00:46:03
    and all plasma cells secrete antibodies
  • 00:46:06
    with identical structure now what these
  • 00:46:08
    antibodies do is they're little
  • 00:46:10
    molecular probes that bind specifically
  • 00:46:13
    to a foreign antigen once that antibody
  • 00:46:17
    binds to a foreign antigen um it
  • 00:46:19
    initiates immune response that we'll
  • 00:46:21
    talk about here in a little bit um but
  • 00:46:23
    once the the infection dies off those an
  • 00:46:26
    and the antigens are cleared
  • 00:46:28
    um there are some memory cells that will
  • 00:46:31
    live on to recognize antigens if you're
  • 00:46:34
    reexposed to that uh you know
  • 00:46:37
    microorganism so activation of B cells
  • 00:46:40
    does require t-h helper cells as well so
  • 00:46:42
    that t- helper cells release sakin that
  • 00:46:45
    also activate B cells and this um
  • 00:46:48
    requires some cellto cell contact
  • 00:46:50
    between B and T cells now the cellto
  • 00:46:53
    cell binding of B and T helper cell
  • 00:46:55
    cells promotes clonal expansion which
  • 00:46:58
    basically means that you can produce
  • 00:46:59
    more clones of these B cells so they can
  • 00:47:02
    divide rapidly and um this can
  • 00:47:05
    proliferate and begin antibody synthesis
  • 00:47:08
    so um what happens you guys is these
  • 00:47:10
    antibodies are also called
  • 00:47:12
    immunoglobulins and they're basically
  • 00:47:13
    just protein chains that are um joined
  • 00:47:17
    by two identical heavy protein chains
  • 00:47:20
    that have what are we called disulfide
  • 00:47:21
    bonds these there's five main classes of
  • 00:47:24
    antibodies
  • 00:47:26
    we have IG IGM IG d and e um IGG is the
  • 00:47:33
    most common it's also the smallest of
  • 00:47:35
    your antibodies so it can really easily
  • 00:47:38
    Escape your bloodstream uh because it's
  • 00:47:40
    so small it's it can really easily slip
  • 00:47:42
    through the spaces between some of the
  • 00:47:45
    cells that line your blood vessels and
  • 00:47:47
    these circulate as single molecules but
  • 00:47:49
    they can enter uh a lot of the
  • 00:47:51
    interstitial fluids of your body now IGM
  • 00:47:54
    is the largest and think about this is
  • 00:47:56
    like the monster so IGM is the monster
  • 00:47:59
    antibody it consists of five antibody
  • 00:48:02
    molecules that are joined together to
  • 00:48:03
    form a pentamer sort of five together
  • 00:48:06
    it's mostly found in your vascular pool
  • 00:48:08
    because it's so big it can't cross the
  • 00:48:09
    capillary wall it's the first to be
  • 00:48:11
    produced upon exposure to antigens and
  • 00:48:14
    it's the major antibody found on B cell
  • 00:48:16
    surfaces and it's one of its main
  • 00:48:18
    functions is to activate compliment we
  • 00:48:21
    learned earlier that once you activate
  • 00:48:23
    compliment that does a variety of things
  • 00:48:25
    like promote the coagulation Cascade um
  • 00:48:29
    attract other immune cells to that side
  • 00:48:31
    of infection but can also activate the
  • 00:48:34
    Mac attack complex which can punch holes
  • 00:48:36
    into foreign cells but it's the IGM here
  • 00:48:39
    once it binds to a foreign cell it can
  • 00:48:41
    actually activate complement that can
  • 00:48:43
    punch a hole in that foreign
  • 00:48:45
    cell IG is a dimer so it's not really
  • 00:48:48
    small but it's going to be larger than
  • 00:48:51
    IGG it's also produced by plasma cells
  • 00:48:54
    that you find in tissue or you know like
  • 00:48:56
    skin and mucous membranes um because
  • 00:48:59
    it's small um you can find IGA in Sal in
  • 00:49:04
    secretions like saliva tears uh in
  • 00:49:07
    mucosal secretions like trob bronchial
  • 00:49:10
    secretions as well as colostrum and
  • 00:49:12
    breast milk now uh you might wonder why
  • 00:49:15
    would you find an antibod in certain
  • 00:49:17
    secretion like saliva tears uh trob
  • 00:49:19
    bronchial secretions and breast milk
  • 00:49:22
    well this antibody can confer immunity
  • 00:49:24
    in that regard so you know saliva has
  • 00:49:28
    antimicrobial aspects because it has
  • 00:49:30
    antibodies in it tears have
  • 00:49:32
    antimicrobial aspects because they have
  • 00:49:34
    antibodies in it and even breast milk
  • 00:49:36
    has some
  • 00:49:37
    antimicrobial aspects because it
  • 00:49:40
    contains its mother's uh antibodies so
  • 00:49:43
    that a newborn gets some immunity due to
  • 00:49:47
    uh you know the absorption of um these
  • 00:49:49
    antibodies from the mother so it's
  • 00:49:51
    pretty cool now igd is found in more
  • 00:49:54
    small amounts in your blood it's located
  • 00:49:57
    primarily on B cell
  • 00:49:59
    membranes and it's thought to be the
  • 00:50:01
    antigen receptor that acts to stimulate
  • 00:50:03
    B cells to multiply differentiate or
  • 00:50:06
    secrete other specific amog globulins so
  • 00:50:09
    igd seems to have more of like a
  • 00:50:12
    regulatory aspect in the immune response
  • 00:50:15
    now this differs from IG because IG
  • 00:50:18
    circulates as a single molecule it's um
  • 00:50:21
    can be bound to basophils and mass cells
  • 00:50:23
    it's found in more Trace Amounts than
  • 00:50:25
    serum
  • 00:50:26
    but it's often involved with immunity
  • 00:50:28
    against helic parasites remember helmets
  • 00:50:31
    are the worm type parasites so IG is
  • 00:50:34
    associated with parasitic infections
  • 00:50:36
    hence the basophil and mass cell
  • 00:50:39
    Association and therefore it's also
  • 00:50:41
    associated with allergic reactions and
  • 00:50:44
    this is believed to be involved as a
  • 00:50:46
    signaling molecule during the parasitic
  • 00:50:49
    and Allergy
  • 00:50:52
    responses now what's interesting though
  • 00:50:54
    is that although these B cells are
  • 00:50:57
    antibody factories they can actually
  • 00:51:00
    produce different types of antibodies so
  • 00:51:02
    antibodies like IGM and igd can be
  • 00:51:05
    switched interchangeably uh between the
  • 00:51:08
    different types of antibodies so it's
  • 00:51:09
    pretty cool so remember IGM is is the
  • 00:51:12
    monster molecule so it's the large one
  • 00:51:14
    and IGM and igd can be switched to other
  • 00:51:16
    smaller ones like g e and a by what we
  • 00:51:19
    call class switching so class switching
  • 00:51:22
    is influenced by the presence of certain
  • 00:51:23
    cyto kindes so you're immune cells can
  • 00:51:26
    alter what types of antibodies you have
  • 00:51:29
    present in your body and that can
  • 00:51:31
    promote a more effective immune response
  • 00:51:34
    and so class sing can be used to
  • 00:51:35
    identify acute versus chronic infections
  • 00:51:38
    so with acute infections you're going to
  • 00:51:40
    find a lot of more uh IGM type of
  • 00:51:42
    antibodies because those are the first
  • 00:51:44
    that are produced however if it's if
  • 00:51:46
    it's a chronic infection you're going to
  • 00:51:48
    be you're going to find a lot more of
  • 00:51:49
    the smaller type of antibodies because
  • 00:51:51
    they've had time to class switch from
  • 00:51:53
    the larger ones like IG and
  • 00:51:56
    igd now you might wonder well what are
  • 00:51:58
    the functions of antibodies you know we
  • 00:52:00
    we called them molecular probes earlier
  • 00:52:04
    and if these are molecular probes what
  • 00:52:05
    are they doing well when these
  • 00:52:07
    antibodies stick to a foreign cell they
  • 00:52:09
    do a couple things for one they can
  • 00:52:12
    precipitate uh cells or substances from
  • 00:52:15
    your body so they can remove substances
  • 00:52:17
    from Body
  • 00:52:19
    Solutions these antibodies can also
  • 00:52:21
    cause cells to uate or Clump together
  • 00:52:24
    and by allowing these foreign cells to
  • 00:52:25
    Clump together they're actually easier
  • 00:52:27
    to remove in that regard now antibodies
  • 00:52:30
    can also neutralize toxins because if a
  • 00:52:32
    toxin's bound up to an antibody it can't
  • 00:52:34
    exert a Toxic effect in a tissue and
  • 00:52:37
    antibodies are also involved with
  • 00:52:39
    opsonization because they can flag a
  • 00:52:42
    foreign cell for phagocytosis so certain
  • 00:52:45
    phagocytes like macrophases and
  • 00:52:47
    neutrophils can specifically remove
  • 00:52:50
    foreign cells that have antibodies stuck
  • 00:52:52
    to them uh but it turns out that
  • 00:52:54
    antibodies can can also activate
  • 00:52:56
    compliment and we know that compliments
  • 00:52:57
    involve with chemot taxis or attracting
  • 00:53:00
    other immune cells uh inflammation as
  • 00:53:02
    well as the membrane attack complex or
  • 00:53:05
    Mac attack complex which basically
  • 00:53:06
    punches holes in foreign
  • 00:53:09
    cells now for the last part of this
  • 00:53:11
    chapter what we're going to wrap up with
  • 00:53:13
    is differentiating passive versus active
  • 00:53:16
    immunity and before we get to passive
  • 00:53:18
    versus active immunity we should Define
  • 00:53:20
    just generally what is immunity well we
  • 00:53:23
    know kind of anecdotally that immunity
  • 00:53:25
    is as a state of resistance against
  • 00:53:28
    infection like if you have an immune
  • 00:53:29
    response then you're resisting infection
  • 00:53:31
    in your body and it's provided primarily
  • 00:53:34
    by adequate levels of antibodies and
  • 00:53:37
    other cells now we talk about the
  • 00:53:39
    concentration of antibodies in your
  • 00:53:41
    serum as being an antibody Tighter and
  • 00:53:43
    if you have a blood test for antibody
  • 00:53:45
    tighter you're basically looking for
  • 00:53:47
    certain antibody
  • 00:53:48
    concentrations and types of antibodies
  • 00:53:51
    which can suggest um different types of
  • 00:53:54
    immunity that's going on on now what's
  • 00:53:57
    interesting is that antibodies can
  • 00:53:59
    achieve both active and passive immunity
  • 00:54:02
    active immunity is actually I'm sorry
  • 00:54:05
    we're going to start with passive
  • 00:54:06
    immunity so passive immunity is the
  • 00:54:08
    transfer of preformed antibodies against
  • 00:54:12
    a specific antigen to an individual so
  • 00:54:16
    an example of passive immunity could be
  • 00:54:18
    like how an infant can receive
  • 00:54:21
    pre-formed antibodies from a mother
  • 00:54:23
    through breast milk
  • 00:54:25
    and we would call that naturally
  • 00:54:27
    acquired passive immunity so because an
  • 00:54:30
    infant is naturally getting uh
  • 00:54:32
    antibodies through a mother's breast
  • 00:54:34
    milk that's a form of naturally acquired
  • 00:54:36
    passive immunity there's also other
  • 00:54:39
    forms of naturally acquired passive
  • 00:54:40
    immunity like for instance a fetus can
  • 00:54:43
    receive antibodies through placental
  • 00:54:45
    transfer so some of the mother's
  • 00:54:48
    antibodies can make it through the
  • 00:54:49
    placenta to Aid in um immunity within a
  • 00:54:54
    fetus
  • 00:54:56
    now there's also something called
  • 00:54:58
    artificially acquired passive immunity
  • 00:55:00
    and if it's artificial that means that
  • 00:55:02
    this is actually being received through
  • 00:55:03
    sort of medical interventions so what's
  • 00:55:06
    interesting is that scientists know how
  • 00:55:08
    to create certain types of antibodies in
  • 00:55:10
    a lab so let's say if you're infected
  • 00:55:12
    with a with a known pathogen like a
  • 00:55:14
    certain type of virus well if you know
  • 00:55:17
    what type of antibody attacks that virus
  • 00:55:20
    or pathogen then scientists can make
  • 00:55:22
    that antibody in lab and then inject
  • 00:55:25
    that specific antibody into someone's
  • 00:55:27
    body to confer an artificial form of
  • 00:55:30
    passive immunity so you can artificially
  • 00:55:33
    inject uh pre-formed antibodies into
  • 00:55:35
    somebody to confer this passive immunity
  • 00:55:38
    so one of the key points with passive
  • 00:55:40
    immunity is that if someone has passive
  • 00:55:42
    immunity they're not making the
  • 00:55:44
    antibodies thems rather they're
  • 00:55:47
    receiving those antibodies from other
  • 00:55:49
    means like if it's if it's natural
  • 00:55:51
    you're receiving it from a mother
  • 00:55:53
    through breast milk or or placental
  • 00:55:56
    transfer and if it's artificial you're
  • 00:55:59
    receiving them in a in a clinical
  • 00:56:01
    setting where you might be injected with
  • 00:56:03
    with antibodies uh to help fight an
  • 00:56:07
    infection now this is used for B cell
  • 00:56:09
    amuno
  • 00:56:11
    deficiencies and um antibody injection
  • 00:56:14
    May alleviate or suppress the effects of
  • 00:56:17
    a particular toxin so when we talk about
  • 00:56:22
    um when we talk about antivenoms that
  • 00:56:25
    kind of stuff or
  • 00:56:26
    antitoxins uh those are often antibodies
  • 00:56:29
    against those toxins that we've
  • 00:56:31
    harvested um through sort of scientific
  • 00:56:33
    means if that makes sense now what one
  • 00:56:36
    important note with passive immunity is
  • 00:56:38
    that it provides immediate but temporary
  • 00:56:42
    Pro protection because if someone's
  • 00:56:44
    receiving pre-formed antibodies outside
  • 00:56:46
    their body like through Brothers I'm
  • 00:56:48
    sorry mother's breast milk or through
  • 00:56:51
    clinical injections you're not training
  • 00:56:54
    their body to learn how to make those
  • 00:56:56
    antibodies on their own they're just
  • 00:56:58
    temporarily receiving those antibodies
  • 00:57:00
    to alleviate that infection however the
  • 00:57:02
    person won't learn how to fight that
  • 00:57:04
    infection on their own so that's one one
  • 00:57:06
    important note with passive
  • 00:57:09
    immunity now there's different types of
  • 00:57:11
    passive immunity like you can get uh
  • 00:57:13
    mother to fetus transfer right so that
  • 00:57:15
    can cross the placenta or mother to
  • 00:57:17
    infant transfer we might have IGA in
  • 00:57:19
    breast milk otherwise you have cotherapy
  • 00:57:22
    where you might have direct injection of
  • 00:57:24
    antibodies into um you know from human
  • 00:57:27
    or animal directly into a patient to
  • 00:57:29
    help fight
  • 00:57:30
    infection now this differs from active
  • 00:57:33
    immunity because active immunity is
  • 00:57:35
    where an individual's own immune system
  • 00:57:38
    can produce its own antibodies against
  • 00:57:41
    infection now this requires memory B
  • 00:57:44
    cells because memory B cells will store
  • 00:57:45
    a memory of that infection and upon an
  • 00:57:48
    SEC second exposure you'll get a quicker
  • 00:57:51
    response so active immunity um would uh
  • 00:57:56
    involve things like
  • 00:57:58
    immunizations because a
  • 00:58:00
    vaccine can stimulate someone's immune
  • 00:58:04
    system to develop immune cells against a
  • 00:58:07
    particular antigen or you know foreign
  • 00:58:11
    protein because vaccines contain foreign
  • 00:58:14
    antigens they stimulate um you know uh
  • 00:58:18
    basically immune responses but they
  • 00:58:20
    don't have pathogenic properties so
  • 00:58:22
    vaccines don't cause disease an
  • 00:58:25
    individual they don't cause harm to the
  • 00:58:26
    host some vaccines contain live or
  • 00:58:29
    attenuated live or attenuated agents but
  • 00:58:32
    they don't cause disease in the host but
  • 00:58:34
    what this does is it it stimulates a
  • 00:58:36
    normal immune response in somebody that
  • 00:58:39
    way they can produce B cells and te-
  • 00:58:41
    cells against an antigen that and they
  • 00:58:44
    can produce their own antibodies against
  • 00:58:46
    that infection and because this
  • 00:58:47
    individual is producing their own
  • 00:58:49
    antibodies we call this active immunity
  • 00:58:52
    now immunizations or vaccines
  • 00:58:55
    are an example of artificially acquired
  • 00:58:58
    active immunity because you're
  • 00:59:00
    artificially injecting a antigen into
  • 00:59:03
    someone's
  • 00:59:05
    body um now what this is showing is the
  • 00:59:08
    difference between the primary versus
  • 00:59:10
    secondary immune response and you can
  • 00:59:12
    see that with the primary immune
  • 00:59:14
    response let's say if we if we are
  • 00:59:16
    exposed to a foreign microorganism it
  • 00:59:19
    can take 10 or more days before we start
  • 00:59:22
    producing antibodies against that micro
  • 00:59:24
    organism remember IGM is the first type
  • 00:59:27
    of antibody that's produced and then you
  • 00:59:29
    can get class switching to smaller
  • 00:59:30
    antibodies like IGG but that takes time
  • 00:59:34
    and so it's important to note that if
  • 00:59:36
    you're first exposed to a foreign
  • 00:59:38
    microorganism it actually takes time to
  • 00:59:40
    develop antibodies against that
  • 00:59:42
    microorganism because with this specific
  • 00:59:45
    adaptive immune response uh it's a
  • 00:59:47
    little bit more slow to develop however
  • 00:59:51
    once you develop immune cells against a
  • 00:59:54
    specific ganogen those immune cells can
  • 00:59:56
    differentiate into memory cells and then
  • 00:59:58
    go dormant in your body which means the
  • 01:00:01
    second time you're exposed to that
  • 01:00:03
    antigen the response is much quicker so
  • 01:00:06
    you can see that instead of taking 10
  • 01:00:07
    days to get antibodies produced it can
  • 01:00:10
    take as little as three days or even
  • 01:00:12
    less to start to produce antibodies
  • 01:00:14
    against that microorganism so the
  • 01:00:16
    secondary response is much quicker and
  • 01:00:19
    much more dramatic so you get more
  • 01:00:21
    antibodies being produced the second
  • 01:00:23
    time but let's talk about this with
  • 01:00:26
    respect to the um you know whole the
  • 01:00:29
    whole idea behind vaccination you know
  • 01:00:31
    vaccination simulates the primary
  • 01:00:34
    stimulus so if you receive a vaccine
  • 01:00:36
    that's like getting a primary immune
  • 01:00:37
    response so you get a vaccine and you
  • 01:00:40
    know the antigens float on your
  • 01:00:41
    bloodstream for some time and then you
  • 01:00:43
    then you develop immune cells that can
  • 01:00:45
    produce antibodies against those
  • 01:00:47
    antigens but let's say that um you know
  • 01:00:50
    those memory cells go dormant but what
  • 01:00:52
    about if if you on the second St
  • 01:00:54
    stimulus what if you were really exposed
  • 01:00:56
    to that microorganism that could cause
  • 01:00:58
    disease well the the first time you're
  • 01:01:01
    exposed to that microorganism is
  • 01:01:03
    actually like the secondary stimulus or
  • 01:01:05
    response because you've already been
  • 01:01:07
    exposed to the antigens of that
  • 01:01:09
    microorganism which means even though
  • 01:01:11
    it's the first time you're being exposed
  • 01:01:13
    to that
  • 01:01:14
    microorganism it's almost like you're
  • 01:01:15
    being exposed for the second time
  • 01:01:17
    because you already have memories
  • 01:01:18
    against against the antigens of that
  • 01:01:21
    microorganism so you get anti body
  • 01:01:23
    production much more more quickly which
  • 01:01:25
    means you have a stronger immune
  • 01:01:27
    response upon exposure to that
  • 01:01:31
    microorganism now one thing that's
  • 01:01:32
    important to note is that vaccines don't
  • 01:01:35
    always confer absolute immunity you know
  • 01:01:38
    just because you you've had a vaccine
  • 01:01:39
    against the particular microorganism
  • 01:01:42
    like influenza or hepatitis uh doesn't
  • 01:01:45
    mean you're totally immune it just means
  • 01:01:47
    that if you are expose your secondary
  • 01:01:50
    immune response here uh will kick in and
  • 01:01:52
    you're going to have a really strong
  • 01:01:54
    immune response which means you're more
  • 01:01:55
    likely to clear off that infection
  • 01:01:58
    before it causes disease
标签
  • Immunity
  • Inflammation
  • Innate Defense
  • Adaptive Immunity
  • Neutrophils
  • Macrophages
  • Complement System
  • Antibodies
  • Vaccines
  • HIV