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Week 4 Concept Questions
Terms in this set (14)
Why isn't immunosuppressive therapy required for blood transfusions?
RBC's do not have nuclei and therefore do not have MHCs
What is the purpose of requiring multiple inputs for activation of T and B-cells?
You HAVE to have signal 1 to activate signals 2 and 3
APCs only provide the signals 2 and 3 if the APC has been activated by PRRs and PAMPs or complements.
*Co-stimulation is often crucial to the development of an effective immune response.
Can the acquired immune response function independently of the innate immune system?
No, they work together.
How would the immune response be affected if MHC class I were not functional on APCs?
Proteasome chops up antigens and normal proteins within the cell into peptides then the peptides bind to MHC I and are displayed on the cell surface which is what looks for antigens.
*Binding affinity can vary greatly, which affects immune activation
MHC I displays peptides 8-12 aa in length
What about if were not functional on other cells in the body? (MHC I)
They would not amount an immune response similar to RBCs?
How would the immune response be affected if MHC class II were not functional on APCs?
MHC class II molecules are critical for the initiation of the antigen-specific immune response.
MHC II typically longer, 13-18 aa's
What about if were not functional on other cells in the body? (MHC II)
MHC II complexes are expressed in APCs
*They would not amount an immune response similar to RBCs?
What do booster injections do for B-cells and antibodies?
Antibody production from a first exposure is detectable 5-7 days after inoculation, peaking 2-3 weeks after first exposure and gradually declining to near 0 levels if the antigen is no longer present
Second exposure causes a precipitous rise in antibody levels within days of exposure, reaching higher levels than in the first exposure and persisting for longer periods of time.
*Leads to the generation of 2nd generation antibodies with improved affinity for the antigen
What would happen to a virus-infected APC?
Some antigens, such as bacterial polysaccharides or repeating determinants on the surface of viruses, are sufficient to activate a B-cell.
CD8 cells lookfor and binds with cells that display the antigen (via MHC I) and kills them.
What cells/systems should work to kill S. aureus and how has S.aureus adapted to work against them?
FPs bind to FP receptors on neutrophils, initiating a signaling cascade which causes chemotaxis to the pathogen, up regulation of receptors to bind bacteria and up regulation of cellular processes to degrade bacteria.
Phagocytosis of bacteria via PRRS or via complement opsonization.
Why are there so many dying neutrophils around an S. aureus infection?
They are ANTI-CHEMOTACTIC which inhibits chemotaxis of neutrophils and prevents neutrophil extravasation
*They also release LEUKOTOXINS that kill neutrophils
*Inhibits ability of neutrophils to move from the blood stream into the interstitial space
Is MSSA more pathogenic than MRSA? If so or not, why?
MRSA and MSSA have similar propensities for their sites of infections
MRSA mortality rates tend to be equal or slightly higher than for MSSA
Would ramping up the adaptive response help improve the immune response against S. aureus?
S. aureus has evolved many mechanisms to disrupt phagocyte function
Adaptive response of antibodies and antibody production is largely intact, but the do have anti-opsonization/phagocytosis properties the inactivate antibodies.
What is the difference between colonization by S. aureus and infection?
Bacterial colonization is the presence of multiplying bacteria without evidence of an immune response
Infection frequently preceded by colonization
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