Ir gene controlled carrier effects in the induction and elicitation of hapten-specific delayed-type hypersensitivity responses.
The genetic requirements of carrier recognition were examined in the priming and elicitation of hapten specific, T-cell mediated, delayed-type hypersensitivity (DTH) responses. It was shown that nitrophenyl acetyl-poly-(L-glu56-L-lys35-L-phe9) (NP-GLO) could prime for NP responses only in strains of mice which are Ir gene responders to GLO. In contrast to this requirement, NO-GLO could elicit an NP-specific response in NP-bovine gamma globulin primed mice, even in GLO nonresponder strains. Furthermore, the nonimmunogenic molecule, NP-GL, could elicit an NP-specific DTH response in animals primed with NP on an immunogenic carrier.
D000818:Animals; D000941:Antigens; D005802:Genes, MHC Class II; D006241:Haptens / Q000276:immunology*; D006968:Hypersensitivity, Delayed; D051379:Mice; D008807:Mice, Inbred BALB C / Q000276:immunology; D008810:Mice, Inbred C57BL / Q000276:immunology; D009578:Nitrobenzenes / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*
D000941:Antigens; D006241:Haptens; D009578:Nitrobenzenes