Activation ofCholera Toxin-Specific T Cells InVitro

1990 
cells (APCs),and various formsofCT-Bas antigen. Theresults indicate thatinmany ways CT-specific T cells respondina manner similar tothat ofTcells specific forother protein antigens: thedegree ofproliferation was proportional tothedoseofantigen andAPCsinthecultures, was antigen specific, andwas H-2restricted. APCsfromgenetic high-responder strains toCTstimulated significantly more proliferation inF1(high x low)responder T cells thandidAPCsfromlowresponder strains. However, there was a markeddifference intheactivation of CT-specffic T cells whendifferent formsofCT-Bwere used.Native CT-Bstimulated little or no T-cell proliferation, whereas denatured CT-Bor CT-Bblocked byitsligand, GM1 ganglioside, stimulated T cells well. Addition ofnative CT-Btococultures ofprimed Tcells, APCs,andthese latter stimulatory formsofCT-B inhibited thespecific proliferative responsetoCT-Btovarying degrees, depending on theratio ofthetwoforms inculture. We conclude thattheability ofCT-Btoinhibit Tcells extends eventoTcells specific forCTitself. Because ofthese inhibitory properties, processing ofCT tononbinding molecular forms orfragments mustbe an important prerequisite fortheimmuneresponsetoCTtooccurinvivo, andsuchprocessing islikely tobe important intheimmuneresponsetoa variety ofotherenterotoxins aswell.
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