Immunology

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Author:
Anonymous
ID:
99500
Filename:
Immunology
Updated:
2011-09-02 13:52:57
Tags:
Hypersensitivity Autoimmunity
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  1. Which parts of the immune system can develop hypersensitivity reactions?
    Humoral and Cell-mediated
  2. When does the immune reaction occur in Type I hypersensitivity?
    After second exposure to the antigen
  3. How soon do Type I reactions occur (Hint: Allergies)?
    A. Delayed
    B. Immediately (minutes)
    C. Intermediate
    B. Immediately
    (this multiple choice question has been scrambled)
  4. What antibody class is responsible for Immediate Hypersensitivity reactions?
    IgE
  5. Put the following steps of Type I rxns in order.
    Cytokines stimulate B cell Ab class switching to IgE, B cell/APC presents Ag to Th2 cell, Activation of mast cells, Th2 secretes cytokines, IgE binds to mast cells, First exposure, Second exposure, Crosslinking of Ag between IgE
    First exposure, B cell/APC presents Ag to Th2 cell, Th2 secretes cytokines, cytokines stimulate B cell Ab class switching to IgE, IgE binds to mast cells, second exposure, crosslinking of Ag between IgE, activation of mast cells
  6. What cytokine stimulates B cell Ab class switching?
    IL-4 from Th2 cell
  7. Th2 cells also release IL-5 and IL-10 in addition to IL-4. What are their functions?
    IL-5 activates eosinophils, IL-10 (along with IL-4) stops macrophage activation
  8. The are two phases to Type I rxns. Describe, in general, what occurs during each phase.
    • Early phase: vascular/ smooth muscle response (histamine major player, released by activated mast cells)
    • Late phase: Inflammation
  9. Three of the four hypersensitivity rxns are mediated by the humoral arm of the immune system. Which one is cell-mediated?
    Type IV
  10. Type II rxns occur due to differences or changes in the Ag on the tissue which the body does not recognize and the B cells (activated by the Ag and Th2 cells) secrete IgG Ab. What are some examples of Type II rxns?
    Blood transfusion rxns, Erythroblastosis fetalis (anti-Rh Ab from mom lyse baby's RBC), penicillin induced
  11. In an immune complex mediated rxn (Type III), what causes the tissue destruction?
    Cells of the innate immune system activated by the immune complex (neutrophils, macrophages)
  12. What is an immune complex?
    An immune complex is a clumping of Ag + Ab (usually IgG) that when it becomes large enough, activates the complement system which activates mast cells to release histamine and recruits/activates innate immune cells
  13. What determines the presentation of disease in Type III rxns?
    The location of deposition of the immune complexes (i.e. endothelial wall -> vasculitis, kidneys -> nephritis, joints -> arthritis)
  14. The Type III rxn that occurs in the skin is called?
    Localized Arthus Reaction (i.e. insect bite)
  15. What cell type initiates Type IV hypersensitivity reactions?
    CD4+ (Th1 helper cells)
  16. Why do Type IV rxns take so much longer to occur than Type I?
    Th1 memory cells are the cells which react to the Ag presented by APC upon second exposure. It can take several hours for the Ag specific T cell to arrive because there is no inflammation to attract T cells so it takes a while for the correct one to arrive. After binding to Ag/MHC complex, the T cells release mediators inducing the inflammatory reaction
  17. What mechanism fails in autoimmune disease?
    Tolerance
  18. What is the difference between central and peripheral tolerance?
    Central tolerance eliminates immature B/T cells that are self-reactive. Peripheral tolerance relates to the mechanisms which abrogate the activity of mature autoreactive B/T cells that escaped
  19. What are the mechanisms of peripheral tolerance for T cells (there are four)?
    • 1. Absence of Signal 2
    • 2. Induction of pro-apoptotic signals when mature T cell binds self-antigen
    • 3. Fas-FasL interactions which induce apoptosis
    • 4. Regulatory T cells
  20. What is Signal 2 in T cells?
    Signal 2 is the binding of CD28 on T cell to B7 ligand on APC (Signal 1 is binding of TCR/CD3 to MHC complex and both are required for naive T cell to become an effector cell)
  21. What is the name for a graft between genetically identical individuals?
    A. xenogeneic
    B. syngeneic
    C. autologous
    D. allogeneic
    B. syngeneic
    (this multiple choice question has been scrambled)
  22. Transplation of what tissue/organ is responsible for graft versus host disease?
    Bone marrow (T cells in bone marrow attack recipient's tissues)
  23. What is the difference between hyperacute and acute rejection of transplanted organs?
    Hyperacute is caused by Ab to ABO or HLA antigens on graft whereas acute is caused by effector T cells responding to HLA antigen differences between graft and recipient
  24. The indirect pathway of allorecognition relates to what type of rejection of transplanted organ?
    Chronic rejection
  25. As a note, there are a few diseases discussed in Dr. Metcalf's lecture on autoimmunity (Sept 1) which might be good to review as some autoimmune diseases are systemic and others are organ specific

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