Adaptive immunity

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Strawberrylotus
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301117
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Adaptive immunity
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2015-04-23 13:41:23
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Ch13
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Ch13
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  1. Characteristics of the Adaptive Immune Response
    Specificity

    Distinguishes between ‘self’ & ‘non-self’ 

    Memory

    Adaptable
  2. differences between innate and adaptive immunity
    • Innate is nonspecific, does not have
    • memory.

    Adaptive is specific and has memory
  3. Adaptive Immunity – 2 Branches
    1. Humoral Immunity       

    2.Cellular Immunity
  4. Humoral Immunity
    •B cells

    •BCR (B cell receptors)

    •Antibodies
  5. Cellular Immunity
    •T cells

    •TCR (t cell receptors)

    •Helper T cells (TH)

    •Cytotoxic T cells (CTL)
  6. Antigen (Ag)
    • protein or polysaccharide recognized by
    • the immune system

    –Examples? flagella, cell wall, pili
  7. Epitopes
    • a subset of a particular Ag, where an Ab
    • or TCR actually bind on the Ag
  8. Antibodies (Ab)
    •Are proteins, immunoglobulins (Ig)

    •Bind to Ag!

    •Made by B cells & plasma cell

    • •Major effector molecule of humoral
    • immunity (meaning that B cells are what
    • the humoral immunity is all about)
  9. What makes antibodies the same?

    What makes antibodies different from eachhother
    1. constant region
  10. What makes antibodies different from eachhother
    the variable
  11. the variable
    The variable areas will be specific to the epitopes on a specific bacteria. They don’t just bind to any bacteria. They will bind to a specific bacteria because they will recognize a specific epitope on that antigen so that is how the interaction will occur
  12. 5 different antibodies
    • iga
    • igg
    • ige
    • igm - most effective at binding antigen. It can bind 10
    • igd
  13. Effects of Antibody Binding
    • 1. Neutralization 
    • 2. Opsonization
    • 3. Oxidation
    • 4. Agglutination
    • 5. Antibody-dependent cellular cytotoxicity (ADCC)
  14. Neutralization
    Antibody can neutrolize the antibody and their toxins by binding to them thereby preventing the bacteria and their toxins to bind to the host cell
  15. Opsonization
    The antigen is coated with antibody in order to enhance ingestion and lysis of bacterium by a phagocyte
  16. Oxidation
    Antibodies have some catalytic properties. Antibodies bind to the bacteria, release hydrogen peroxide killing the cell
  17. Agglutination
    Antibody and antigen clumping making it easier for it to be ingested by a phagocyte.

    Igm most effective for agglutination.
  18. Antibody-dependent cellular cytotoxicity (ADCC)
    The antibody will bind to the antigen but the fc portion of the antibody will be bound by a natural killer cell. And upon this interaction this nk cell is going to release perforin and granzyme. it enters the cell and it triggers the cell to induce apoptosis (self destruct).
  19. Major Histocompatibility Complex (MHC)
    •Receptors found on all cells except RBCs

    •Also known as human leukocyte antigen (HLA)

    • •Plays a role in recognition of self by the immune system and in rejection of foreign
    • tissue
  20. Major Histocompatibility Complex (MHC) 2
    • People receiving transplants they don’t only look at your blood type they look at your
    • MHC too. They are receptors that are found on all cells in your body except red blood cells.
  21. Genes for MHC clustered in a multigene complex
    Class l

    Class ll
  22. Class 1
    –markers that display unique characteristics of self molecules and regulation of immune reactions

    •required for T lymphocytes

    - found in all nucleated cells
  23. Class 2
    • –receptors that recognize and react with foreign antigens; located primarily on
    • macrophages and B cells

    - involved in presenting antigen to T-cells

    - found in antigen presenting cells such as macrophages, dendritic cells, and B cells
  24. Lymphocyte Receptors
    •Lymphocyte’s role in surveillance and recognition is a function of their receptors.

    •B-cell receptors – bind free antigens

    •T-cell receptors – bind processed antigens
  25. Activation of B Cells
    1.Bind antigen

    2.Internalize antigen

    3.Process and express antigen on MHC class II molecules
  26. Activation of B Cells 2
    1. Helper T cell recognized antigen on MHC class II molecule and produces cytokines to help activate B cells *

    • 2. B cells proliferate & differentiate
    • into:
    •      a.Plasma cells
    •      b.Memory cells
  27. Activation of B Cells
    T-dependent antigen – most proteins

    • –B cells need Ag to also be recognized by
    • T cells (confirmation that the Ag is indeed foreign)

    • –B cells cannot become fully activated
    • until a T cell recognizes the Ag presented in MHC class II molecules & secretes cytokines
  28. T-independent antigen
    large polysaccharides

    –Have repeating structures / subunits

    –Bind multiple BCR’s

    • –B cells do not need T cell help to become
    • fully activated
  29. B Cell Clonal Selection
    • •Each B cell will recognize only 1 Ag, and
    • will make Abs that only bind this 1 Ag

    • •The BCR on the surface of B cells is what
    • binds to this 1 Ag (made up of Abs on the surface of the B cell)
  30. B Cell Clonal Selection 2
    • •In response to infection only B cells who
    • can recognize the Ag (BCR-Ag binding) will become activated

    –A small % of the total # of B cells

    –All B cells are NOT activated during infection

    •Through activation clonal ‘armies’ are made as only B cells that recognize Ag proliferate
  31. Antibody Production
    •1st Abs produced is class IgM, IgG is made later

    • •The levels of Abs and specific Abs can be
    • measured in the serum (liquid portion of blood)
  32. Antibody Production 2
    • •Ab levels can be used to monitor the immune response
    •      –Antibody titer

    • •A secondary/ memory response will produce
    • Abs more quickly and in greater quantity
  33. Antibody titer
    •Ab levels can be used to monitor the immune response
  34. Humoral Immunity
    • is effective against pathogens in circulation, or outside the cell
    •      –Bacteria, viruses, parasites, etc.
  35. Cellular Immunity
    • •provides a means of destroying intracellular pathogens, inside the cell
    •      –Intracellular Ag are not exposed to Abs
    •      –Infected cells must be detected and killed to clear some infections
  36. Helper T cells (TH)
    •coordinate / direct immune responses

    • •Identified by CD4
    • glycoproteins on surface of cells
  37. TH1
    Responds to most bacterial & viral pathogens; activate macrophages, activate Cytotoxic T cells
  38. TH2
    Respond to parasites and involved in allergies; activate B cells
  39. T-regs
    Regulates T cell responses, can put the ‘brakes’ on the immune response
  40. Cytotoxic T cells (CTL)
    •Kill host cells infected with intracellular pathogens

    •Identified by CD8 glycoproteins on the surface of cells
  41. T cells
    • • Must be educated and learn the antigens
    • present on a pathogen before they can attack!

    • • T cells are educated by Antigen Presenting
    • Cells (APC)
  42. 2 main Antigen Presenting Cells
    dendritic cells & macrophages
  43. Antigen Presenting Cells
    •APC’s display Ags to T cells on MHC molecules on the outside surface of the APC

    –MHC Class I molecules recognized by CTL (CD8+ T cells)

    • –MHC Class II molecules recognized by TH
    • cells (CD4+)
  44. T cell Education
    •Requires direct interaction with APC

    •Takes place in secondary lymphoid organs

    •APC patrol the body and phagocytose microbes, debris, & dead cells
  45. T cell Education 2
    •Once APC’s ‘eat’ something and are activated they go to the nearest 2 degree lymphoid tissue to display Ags to T cells

    • –APC’s are activated through binding of
    • Toll-like receptors; or by cytokines (produced by WBC’s & other cells)
  46. Cytotoxic T cell Killing
    • •Distinguish between antigens from intracellular pathogens and the host cell presented on
    • MHC class I molecules 

    • •CTL’s then are activated to release molecules that induces apoptosis in the target
    • cell
    •      - Perforin
    •      - Granzyme
  47. CTL Killing - Apoptosis
    programmed cell death, changes occur in the cell membrane to signal phagocytes to ingest them.  Different from necrosis where cells lyse and their contents are released into extracellular space.
  48. Perforin
    enzyme that makes pores in the cell membrane
  49. Granzyme
    proteases that induce apoptosis
  50. Antibody-dependent cell-mediated cytotoxicity (ADCC)
    • NK Cells recognize when Abs have bound to a
    • microbe by recognizing the Fc-region of the antibody via Fc receptors

    –Upon binding Abs via their Fc receptors, NK cells release perforin & granzymes which kill the target cell

    • –NK cells do not learn each pathogen specifically!
    •      •NK cells recognize when Abs are bound to microbes (here the Ab is specific & the NK cell recognition is nonspecific)
    •      •CTL’s recognize specific Ags on MHC class I of infected cells
  51. Cytokines
    • Soluble molecules released mainly by
    • leukocytes to communicate and coordinate /

    Directs the immune response
  52. Cytokines 2
    –Interleukins (IL-1, IL-2, etc.)

    –Chemokines: signals for leukocyte extravasation and migration within tissues (chemotaxis)

    –Interferons (IFN-y)

    –Tumor necrosis factors (TNF-a)
  53. ch12 pg34
  54. T helper cell 1
    receptors: CD4

    activates the cell-mediated immunity pathway, secretes tumor necrosis factor and interferon gamma, also responsible for delayed hypersensitivity (allergy occuring several hours or days after contact)
  55. T helper cell 2
    recepter CD4

    drives B-cell proliferation, secrete IL-4, IL-5, IL-6, IL-10; can dampen TH1 activity
  56. T cytotoxic cell (Tc)
    receptor CD8

    Destroys a target foreign cell by lysis, important in destruction of complex microbes, cancer cells, virus-infected cells; graft rejection; requires MHC 1 for function
  57. Generalized immune response of leukocytes accumulating at the site of infection (part 1)
    1)Expansion of immune cells

    •Cells become activated & proliferate

    • •Clonal activation of only those T cells & B cells that recognize the particular Ags
    • of the pathogen
  58. Generalized immune response of leukocytes accumulating at the site of infection (part 2)
    2) Retraction of immune cells

    •Cells undergo apoptosis

    • •A small portion of T cells & B cells will remain as memory cells so that the
    • next time the pathogen is encountered the immune response will be faster &
    • stronger!

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