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ImmunologyParasiteDz
lecture 31 niederkorn
Question | Answer |
---|---|
cercaria | the larval stage of schistosomes released by snails into fresh water |
schistosomula | infectious skin stage of schistosomes; arises from cercariae that penetrate the skin |
concomitant immunity | occurs when immune system is able to fend off a re-infection a specific helminth (like schistosomula) but can't get rid of the worms that are still in the body from first infection |
hallmark of helminth infections | eosinophilia, elevated levels of IgE |
critical period for immune system effect with response to Schistosomes | immune system must execute eradication within 24-36 hrs. after 48 hrs they move to mesenteric veins and are impervious to the immune system |
process of concomitant immunity | hyper IgE after initial infection, armed mast cells and eosinophils. new infection activates mast cells --> degranulation and cytokine storm (ECF) for influx of eosinophils that do ADCC using cationic proteins |
ADCC (antibody-dependent cellular toxicity) | specific IgE FcR against helminths are bound to eosinophils, whenever they invade and IgE binds the schistosomula, eosinophils can then irreversibly bind & kill |
Th2 cells secrete IL-4 and IL-5 for immediate hypersensitivity upon re-infection | IL-4 = IgE class-switching IL-5 = eosinophil chemoattractant |
primary mechanism of eradication of Toxoplasma | killing by activated macrophages that phagocytose IgG-coated Toxoplasma (opsonization) |
primary cells for immunity after initial Toxoplasma infection | Th1 cells are activated and start secreting IFN-gamma, which activates macrophages |
reservoirs for latent Toxoplasma infection | cells which do not have MHC class I expression like brain and eye (immunoprivileged sites) |
immunity to liver stage of Plasmodium and Toxoplasma infections | hepatocytes express Ag on their MHC class I, which is recognized by CD8+ T cells specific for infecting protozoan; IFN-gamma = NO production and killing |
Plasmodium: sporozoites vs hypnozoites vs merozoites | sporozoites - released from Anopheles mosquito after bite, they home to liver cells; hypnozoites - protozoal form that can be dominant in liver cells for yrs; merozoites - form that is released from liver cells to infect RBCs |
immunity to Plasmodium sporozoite stage | opsonization and ADCC must occur QUICKLY b/c entire body blood vol passes through liver in minutes and after arriving, they enter and infect quickly |
immunity to Plasmodium merozoites that have infected RBCs | RBCs express Ag naked on surface (NOT BY MHC class I), opsonization and ADCC in reticuloendothelial system of liver and spleen |
clearance of re-infection of Trichinella (or other gut-dwelling roundworm) | initial infection stimulates Th2 response that mediates complete clearance the second time around within 7 days |
body's immune response/physiological changes as a result of Trichinella infection | proliferation of gut mast cells with Trich-specific IgE loaded, hyperplasia of goblet cells and increased mucus secretion with IgA to bind them, dramatic gut motility increase, eosinophilia |
how Trichinella larvae in muscle are cleared | they can't be cleared, usually cause myositis due to eosinophil infiltrate, eventually larvae are calcified within muscle |
mechanisms for parasite escape | antigen variation using up to 1000 variable surface glycoproteins + escaping phagosome (both in Trypanosoma!), prevention of phago-lysosomal fusion (Toxoplasma), being impervious to lysosomal enzymes (Leishmania) |
example of organ that exhibits Ag mimicry | Schistosoma and Plamodium falciparum acquire ABO blood group antigens and MHC antigens thus appearing to be host cells; are weakly immunogenic and impervious to conventional immune effector mechanisms |
Th1 cells | activate macrophages by releasing IFN-gamma to have protective immunity against protozoa, especially Leishmania |
Th2 cells | are activated by helminth infections to release IL-4 and 5 for eosinophils to do their work |
Th17 cells | important in bacterial infections |
real cause of river blindness from Onchocerca infection | Th2 cell response to larval antigens is toxic to the ocular surface, chronic inflammation damages it |