Synergistic genetic defect in B-lymphocyte function. I. Defective responses to B-cell stimulants and their genetic basis.
CBA/N female mice, which express an X-linked defect in B-lymphocyte function, were mated with C3H/HeJ male mice, which are unresponsive to lipopolysaccharide (LPS). The resulting F1 hybrid females were mated to C3H/HeJ males. Approximately one-half of the backcross (BC.1) males obtained from this mating expressed a more profound immunologic defect than either of the parental strains. Spleen cells from these mice were unresponsive to a series of B-cell mitogens including LPS prepared from Escherichia coli K235 and from E. coli 0111:B4, lipoprotein mitogen from E. coli, and Nocardia water-soluble mitogen (NWSM). They failed to give in vitro antibody responses to the thymus-independent type 2 (TI-2) antigen trinophenylated Ficoll and most were unresponsive to the TI-1 antigens trinitrophenylated Brucella abortus, trinitrophenylated LPS, and trinitrophenylated NWSM. This synergistic defect in B-lymphocyte function depended on the presence of the CBA/N xid gene but the critical gene(s) from the C3H strain was not the defective Lps gene (Lpsd). These mice should provide a valuable tool for the elucidation of B-lymphocyte ontogeny, heterogeneity, and function.
D000818:Animals; D000917:Antibody Formation; D001402:B-Lymphocytes / Q000276:immunology*; D001426:Bacterial Proteins / Q000276:immunology; D003433:Crosses, Genetic; D004140:Dinitrophenols / Q000276:immunology; D005260:Female; D006433:Hemocyanins; D007125:Immunogenetics; D008070:Lipopolysaccharides / Q000276:immunology; D008213:Lymphocyte Activation; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D008808:Mice, Inbred CBA
D001426:Bacterial Proteins; D004140:Dinitrophenols; D008070:Lipopolysaccharides; D006433:Hemocyanins