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43 Cards in this Set

  • Front
  • Back
What cytokines dominate the Th1 response?
INF-gamma and IL-2.
What cytokine will cause a Th0 cell to become Th1?
What cytokines are activated in a Th1 cell release?
IL-2 (for self and others) and INF-gamma.
Which cytokines are suppressed by IL-2 and INF-gamma?
IL-4 and IL-13, which result in the Th2 response.
What is the purpose of INF-gamma?
Activate macrophages.
Which cytokines promote B-cell proliferation?
IL-4, IL-10 (potent downregulator of Th1), IL-13.
What cytokine promotes isotype switching?
IL-4, IL-10.
What are the Th1 initiation steps?
Pathogen is binds to a TLR on the DC.
What cytokine is released by an activated macrophage to stimulate Th1 development?
What is required in the propagation and maintenance of the Th1 response?
IL-2 is a growth factor that helps to sustain and produce activated Th1 cells.
What is the normal result of a Th1 response?
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.
What occurs during an unregulated Th1 response with a defective macrophage?
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.
What is a granuloma?
A frustrated TMMI response. Th1 cells and macrophages are overactivated, resulting in the destruction of tissue rather than the pathogen.
What will occur if a patient has defective TMMI?
Pathogen will persist intracellularly and no macrophages will be activated.
What is the step by step sequence of the TMMI response?
Review this in the notes.
What occurs during the cytotoxic response?
(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.
What happens in an HIV patient?
Patient has no CD4, so no priming will occur and no INF-gamma will be released.
What happens to CD8 cytotoxicity when Th1 response is defective?
(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.
What is the normal response to a pathogen when the APC is a B-cell?
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.
What is the function of IL-4?
To promote the Th2 response as well as to suppress the Th1 response.
What is the logic behind the Th2 response?
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)
How does the Fc-R response work?
In all scenarios but one, the Ab must be bound to the Ag and then crosslink to IgG.
What is the result of IgG crosslinking with Fcγ-R, with regard to Ig production?
ITIM signal is sent to the B-cells - downregulation of the production of IgG (which is different if FcM-R).
What is the result of Mac/DC cross linking with Fcγ-R?
ITAM - more are activated.
What is the result of neutrophils cross linking with Fcγ-R?
ITAM - more are activated.
What is "arming" of the Fcε-R?
VERY HIGH affinity receptors can cross link to mast cells and basophils without the bound Ag-Ab complex. This is only in allergy.
What is a Type III hypersensitivity diseaes?
Excess immune complex disease.
What receptors are involved in immune complex diseases?
Fcγ-R and C3b-R.
What three locations are prime targets for attack in immune complex diseases and why?
Skin, kidney, and synovial joints because they have abundant Fcγ-R and C3b-R.
What arm of the immune system is persistent throughout life?
Innate immune system.
What happens to a B-cell antigen when the B-cell is absent?
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.
What happens to a B-cell antigen when the B-cell is present but defective?
Ag presentation may occur, but there will be no plasma cells. B-cells will respond abnormally to growth and switching signals.
What happens to a B-cell antigen when the T-cell is absent or defective?
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.
What is Type I hypersensitivity disease?
Allergic response.
What is absolutely required in every patient that has allergies?
Genetic predisposition to allergies.
What is the main problem that causes an allergic response?
There is no isotype switch from IgE to IgG.
What is the sequence of events in the first allergic response?
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.
Which cytokine drives the isotype switch to IgE?
IL-4 and IL-13.
How does a Th0 -> Th2 conversion occur?
Presence of IL-4, or absence of IL-12.
What is the sequence of events in the second allergic response?
Massive inflammation by armed basophils and mast cells. See notes.
What is the function of eosinophils in the allergic response?
It is the late response that produces prolonged inflammation.
What cytokine is related to recruiting eosinophils?
What occurs when a superantigen activates the Th1 response?
Superantigen binds to the OUTSIDE of the MHC complex, activating an inordinate amount of INF-gamma. Nearly all the macrophages in the area