Flashcards in 11/8/12 Deck (21):
what types of pathogens are intracellular?
some bacteria and protozoa
what is main defense against intracellular pathogens?
cytotoxic t lymphocytes
what receptors are on NK cell surface and what stimulates them?
activating receptor = NKG2D. Recognize MIC
inhibitory receptors on cell surface - recognize MHC I receptor
what is the main defense against extracellular pathogens?
helper T cells
what cell type activates macrophage to kill organisms ingested?
how do Th1 cells enhance killing of organisms ingested by phagocytes?
binds MHCII and becomes activated
upregulates CD40 and produces IFNgamma
activates production of ROS in phagocyte endosomes
how do Th1 and Th2 and B cells facilitate pathogen uptake and breakdown in macrophages?
Th1 and Th2 help B cells produce high affinity Abs that facilitate pathogen uptake
activate macrophages via Fc receptors
what is the response to helminth infections?
produces IL-4, IL-13 which are recognized by epithelial cells on mucosal surface
cytokines stimulate eosinophils
what is the mucosal cell response to IL-4 and IL-13 in helminth infection?
increase turnover helps shed parasitized cell
mucus prevents adherence and accelerates loss of parasite
how do eosinophils get activated and respond to helminth infection?
IL-4 promotes IgE production by B cells
IgE targets helminth
eosinophils become cytotoxic
General mechanism of type I hypersensitivity?
similar to anti-helminth response
general mechanism of type II
involves antibodies binding to surface-linked antigens.
general mechanism of type III
antibodies binding to soluble antigens
general mechanism of type IV
depends on activation of antigen-specific T cells
what is the most effective anti-tumor function of the immune system?
what types of antigens would a tumor cell present to CTLs triggering their activation?
1. presention of mutant peptide from mutated cellular protein
2. reactivation of embryonic genes not normally expressed in differentiated cell
3. overexpression of normal self protein changing density of self-peptide presentation
how do innate lymphocyts recognize tumor cell?
increased MIC expression on tumor cell
NGK2d receptor on NK or gammadelta cell activate cytotoxicity
In general, how do tumor cells avoid immunosurveillance?
those cells that mutate and have way to evade win out
what are the two main ways tumor cells avoid immunosurveillance?
how does immune evasion work and give example
loss of expression of things that killer cells recognize
i.e. variant tumor cell cleaves MIC (becomes soluble) or blocks expression of MIC