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43 Cards in this Set
- Front
- Back
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What cytokines dominate the Th1 response?
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INF-gamma and IL-2.
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What cytokine will cause a Th0 cell to become Th1?
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IL-12.
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What cytokines are activated in a Th1 cell release?
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IL-2 (for self and others) and INF-gamma.
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Which cytokines are suppressed by IL-2 and INF-gamma?
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IL-4 and IL-13, which result in the Th2 response.
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What is the purpose of INF-gamma?
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Activate macrophages.
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Which cytokines promote B-cell proliferation?
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IL-4, IL-10 (potent downregulator of Th1), IL-13.
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What cytokine promotes isotype switching?
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IL-4, IL-10.
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What are the Th1 initiation steps?
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Pathogen is binds to a TLR on the DC.
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What cytokine is released by an activated macrophage to stimulate Th1 development?
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IL-12.
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What is required in the propagation and maintenance of the Th1 response?
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IL-2 is a growth factor that helps to sustain and produce activated Th1 cells.
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What is the normal result of a Th1 response?
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Macrophages are activated by the inflammatory tetrad to destroy intracellular antigen. Hydrolases and oxidases are also activated.
MHC's are also upregulated on the surface. |
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What occurs during an unregulated Th1 response with a defective macrophage?
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Too much INF-gamma is being produced because the antigen persists. Overactivation of frustrated macrophages are produced and will kill host tissue, the hypersecretion of the inflammatory tetrad will also cause problems systemically.
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What is a granuloma?
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A frustrated TMMI response. Th1 cells and macrophages are overactivated, resulting in the destruction of tissue rather than the pathogen.
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What will occur if a patient has defective TMMI?
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Pathogen will persist intracellularly and no macrophages will be activated.
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What is the step by step sequence of the TMMI response?
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Review this in the notes.
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What occurs during the cytotoxic response?
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(Review this in notes, this may not be right.)
1) NK cells activated by altered MHC I. 2) DC's prime a CD8 response that will seek out and kill antigens. 3) CD4 will release IL-2 and INF-gamma to promote the Th1 response. |
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What happens in an HIV patient?
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Patient has no CD4, so no priming will occur and no INF-gamma will be released.
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What happens to CD8 cytotoxicity when Th1 response is defective?
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(Review this in notes.)
Only NK cells are available to kill the pathogen, and severe illness results. CD4's do not release IL-2 and INF-gamma so CD8 T cells are not activated. DC's also do not prime CD8 cells. |
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What is the normal response to a pathogen when the APC is a B-cell?
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This can only be activated by an extracellular antigen, which will cause the B-cell to release IL-4 and switch to a Th2 response. This will stimulate B-cells to become plasma cells, which will then release Ab's specific to the bacterial toxin.
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What is the function of IL-4?
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To promote the Th2 response as well as to suppress the Th1 response.
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What is the logic behind the Th2 response?
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Produce Ab's that will bind to extracellular antigens, which will then recruit neutrophils and macrophages to destroy the cell via C3b-R and Fc-R cross linking.
(review this in notes also) |
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How does the Fc-R response work?
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In all scenarios but one, the Ab must be bound to the Ag and then crosslink to IgG.
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What is the result of IgG crosslinking with Fcγ-R, with regard to Ig production?
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ITIM signal is sent to the B-cells - downregulation of the production of IgG (which is different if FcM-R).
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What is the result of Mac/DC cross linking with Fcγ-R?
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ITAM - more are activated.
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What is the result of neutrophils cross linking with Fcγ-R?
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ITAM - more are activated.
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What is "arming" of the Fcε-R?
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VERY HIGH affinity receptors can cross link to mast cells and basophils without the bound Ag-Ab complex. This is only in allergy.
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What is a Type III hypersensitivity diseaes?
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Excess immune complex disease.
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What receptors are involved in immune complex diseases?
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Fcγ-R and C3b-R.
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What three locations are prime targets for attack in immune complex diseases and why?
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Skin, kidney, and synovial joints because they have abundant Fcγ-R and C3b-R.
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What arm of the immune system is persistent throughout life?
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Innate immune system.
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What happens to a B-cell antigen when the B-cell is absent?
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Plasma cell deficiency - results in no Ag presentation, no Ab production, no phagocytosis facilitated by B-cell presentation. The result is a persistent infection from encapsulated bacteria.
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What happens to a B-cell antigen when the B-cell is present but defective?
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Ag presentation may occur, but there will be no plasma cells. B-cells will respond abnormally to growth and switching signals.
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What happens to a B-cell antigen when the T-cell is absent or defective?
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Ag presentation will occur, and IgM's will be produced by plasma cells (hyper-IgM syndrome). However, no IgG's will be present because no isotype switching can occur without T-cells. B-cells are T-cell dependent and require that TCR's recognize the same antigen in order for cytokines to be released that stimulate isotype switch (IL-4 and IL-10). No B-cell activation, no plasma cells, no facilitated phagocytosis.
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What is Type I hypersensitivity disease?
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Allergic response.
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What is absolutely required in every patient that has allergies?
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Genetic predisposition to allergies.
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What is the main problem that causes an allergic response?
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There is no isotype switch from IgE to IgG.
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What is the sequence of events in the first allergic response?
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1) Allergen is prsented by DC's TLR.
2) Th0 -> Th2 (suppressing Th1) and IL-4 is released. 3) B-cells differentiate into plasma cells. 4) Plasma cells synthesize IgE's. 5) Mast cells and basophils are armed for an allergic response in subsequent exposures to allergens. |
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Which cytokine drives the isotype switch to IgE?
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IL-4 and IL-13.
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How does a Th0 -> Th2 conversion occur?
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Presence of IL-4, or absence of IL-12.
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What is the sequence of events in the second allergic response?
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Massive inflammation by armed basophils and mast cells. See notes.
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What is the function of eosinophils in the allergic response?
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It is the late response that produces prolonged inflammation.
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What cytokine is related to recruiting eosinophils?
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IL-5.
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What occurs when a superantigen activates the Th1 response?
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Superantigen binds to the OUTSIDE of the MHC complex, activating an inordinate amount of INF-gamma. Nearly all the macrophages in the area
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