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21 Cards in this Set

  • Front
  • Back
What key mechanism dictates the host response to an antigen?
MHC-antigen presentation.
Why does an antigenic peptide presented by a MHC have almost infinite flexibility with disease expression and symptom variability?
Extremely polymorphic MHC, TLR, and cytokine genes produce unique and extensive repertoires per individual.
Why do some people react differently to the same vaccine?
Extreme heterogeneity of TLR, MHC, and cytokine genes.
What role does IL-10 play in bone marrow transplants?
It suppresses the Th1 response, thus lower the incidence of transplant organ rejection by GvH disease.
How are superantigens different from classical antigens? Name 3 differences.
1) Elicit a massive, immediate primary T cell response.
2) React with MHC II in an UNPROCESSED form. No antigen uptake and processing involved.
3) Do not attach to TCR's peptide binding groove, but on the "side" of the MHC II-TCR complex - such unconventional binding can activate 30% of peripheral T-Cells.
What is a "toxic shock syndrome"?
A superantigen toxin activates rapid T cell proliferation, which release massive inflammatory cytokines (cytokine storm) resulting in toxic shock syndrome and severe perturbations in organ function.
What cytokines are involved in toxic shock syndrome?
INF-gamma from Th1 cells.
TNF-alpha from macrophages.
In a general sense, how do virus superantigens survive in the host?
By hijacking host genes and shut off the host's alarm systems.
How do bacteria/virus superantigens evade the innate immune response?
Downregulate the Toll-like Receptors.
How do superantigens evade CD8 cytotoxic T-cells?
By interfering with the MHC I presentation, effectively camouflaging the superantigen from the CD8 T-cells.
How do superantigens evade NK cells?
They pirate the genes that produce inhibitory signals for NK cells that keep them shut off.
How do superantigens evade the inflammatory response?
They overtake genes that code for IL-10, also IL-12, and any other suppressors of inflammation.
How do superantigens evade the cytokines that have already been by the immune response and released into the circulation?
Encode genes that produce soluble cytokine receptors, blindfolding them from their target effector receptors.
How do superantigens block apoptosis?
Interfering with CASPASE activation or suppressing Bcl (anti-apoptotic) activity.
How do parasitic superantigens avoid the immune response?
Inactivate DC's, switch on the Th1 pathway, and prevent IgE production.
Some superantigens may also induce CD4,25 T-reg cells to suppress an immune response.
What gender bias exists in autoimmune disease? Why?
Occurs predominantly in females.

Females express specific sex hormones (estrogen and progesterone), have more vigorous Th1 responses, and more vigorous Ab responses.
What 3 genetic factors exist to enhance one's susceptibility to autoimmune disease?
1) Monozygotic twins - one develops autoimmune disease, the other is at higher risk.
2) DR (and TLR and cytokine) alleles affect the intensity and composition of Ag presentation.
3) Apoptotic genes - decreased apoptosis means decreased elimination of self-reactive cells.
What are the 2 major mechanisms of self-tolerance? Describe each.
1) Central tolerance - negative selection of self-reactive thymocytes in the thymus.
2) Peripheral tolerance - CD4,25 FoxP3 T-reg cells shut off autoreactive cells in the periphery that have escaped deletion in the thymus.
What is the result of a complete absence of the AIRE (AutoImmune REgulator) complex?
No self peptides for organs surface antigens are expressed in the thymus and all autoreactive cells are allowed to escape to the periphery, destined to attack self.
What is the result of a defect in FoxP3 gene or loss of functional CD4,25 T-reg cells?
Loss of peripheral tolerance and increases in autoreactive T and B cells.
How does the thymus prevent autoimmunity?
By sifting developing thymocytes through autoimmune screening cells that present self-antigens similar to those found on the surface of the individuals organs, and any thymocyte with too much affinity will be negatively selected.