Lipopolysaccharide-induced IgM production is not suppressed by antigen receptor ligation in B cells from some autoimmune strains of mice.

Ligation of surface immunoglobulin on resting or activated nonautoimmune B cells inhibited lipopolysaccharide (LPS)-induced total IgM production. B cells from NZB, (NZB x NZW)F1, and BXSB mice were relatively resistant, but B cells from NZW or MRL/lpr mice were inhibited. The resistance occurs in B cells from young and old NZB mice, and in both resting and activated splenic NZB B cells. Anti-ssDNA responses induced by lipopolysaccharide occur in the presence of antigen-receptor-ligating antibody in NZB, but not in DBA/2, B cells. Antagonism in signaling between the antigen and LPS receptor is not a general B cell hyporesponsiveness, but defects in antagonism specifically between antigen and LPS signaling may be a predisposing factor to autoimmune disease in some autoimmune strains of mice.