Phosphorylcholine-specific helper T cells in mice with an X-linked defect of antibody production to the same hapten.
F1 male mice with the CBA/N X-linked defect that are unable to produce plaque-forming cell responses to phosphorylcholine (PC) provide normal PC-specific helper T-cell activity when compared to F1 female littermates. Inhibition of helper activity with anti-idiotypic antiserum indicates that PC-specific T cells from both NBF1 female and male mice possess predominantly BALB/c myeloma protein HOPC-8 idiotypic determinants. Therefore, the CBA/N defect cannot be explained as a deletion of genes coding for V-region anti-PC specificities. The demonstration of helper activity in NBF1 male mice, which occurs in the absence of anti-PC antibody synthesis, also demonstrates the endogenous origin of the T-cell receptor.
D000818:Animals; D000917:Antibody Formation; D001402:B-Lymphocytes / Q000276:immunology*; D002794:Choline / Q000031:analogs & derivatives*; D005260:Female; D005796:Genes; D008040:Genetic Linkage; D006241:Haptens; D007130:Immunoglobulin Idiotypes / Q000235:genetics; D008211:Lymphocyte Cooperation; D051379:Mice; D010767:Phosphorylcholine / Q000276:immunology*; D011828:Radiation Chimera; D013601:T-Lymphocytes / Q000276:immunology*; D014960:X Chromosome
D006241:Haptens; D007130:Immunoglobulin Idiotypes; D010767:Phosphorylcholine; D002794:Choline