Synergistic genetic defect in B-lymphocyte function. I. Defective responses to B-cell stimulants and their genetic basis.

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Abstract
CBA/N female mice, which express an X-linked defect in B [bone marrow-derived] 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 1/2 of the backcross (BC.1) males obtained from this mating expressed a more profound immunologic defect than either parental strain. Spleen cells from these mice were unresponsive to a series of B cell mitogens including LPS prepared from Escherichia coli K235 and 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 elucidation of B-lymphocyte ontogeny, heterogeneity and function.