The specific B cell subset lacking in the CBA/N mouse is not required for the production of autoantibody in (CBA/N x NZB)F ₁ male mice

Abnormalities in B cell function, which may lead to immunoglobulin (Ig) hypersecretion and autoantibody production, have been implicated in the autoimmune disease of the NZB mouse and its hybrid strains. In sharp contrast to the NZB, the CBA/N strain is deficient in its reponse to a number of antigens due to an X-linked recessive defect manifested by the deficiency of a subpopulation of mature B cells. In the studies reported here, (CBA/N x NZB)F ₁ mice were used to examine the importance of this B cell subset, lacking in the CBA/N, in the development of autoimmune disease in the NZB. As expected, the (CBA/N x NZB)F ₁ female did not express the CBA/N defect, and was similar to other NZB heterozygotes in that it exhibited hypersecretion of Ig and the development of anti-erythrocyte and anti-DNA antibodies. The F ₁ male, in contrast, expressed the CBA/N defect, as represented by diminished spontaneous Ig secretion and the absence of a response to TNP-AECM-Ficoll. However, a number of these mice were still able, although to a lesser degree than the F ₁ females, to produce both anti-erythrocyte and anti-DNA antibodies. These findings indicate that the B cell subset lacking in the CBA/N is important for overall immunoglobulin secretion and the development of antibodies to a particular subgroup of antigens, even in the presence of autosomal NZB genes promoting hypersecretion of immunoglobulin. However, this B cell subset is not absolutely required for the production of at least two specific autoantibodies.