BXSB male mice, which spontaneously develop a systemic lupus erythematosus (SLE) like disease, were the only strain to have a significant incidence of abnormally elevated levels of gp70 in sera. Concentrations of gp70 in some mice were more than 10 times (greater than 500 micrograms/ml) those of young BXSB and any other murine strain. The presence of high serum levels of gp70 was significantly associated with hepatic sinusoidal lymphocytosis, a high incidence of which was only observed in male BXSB mice. Serum levels of gp70-anti-gp70 immune complexes were greatly increased in mice with high levels of gp70, presumably associated with increased anti-gp70 antibody production. Such mice developed fatal glomerulonephritis significantly earlier than those with lower levels of gp70. These results suggest that (1) hepatic inflammation of unknown aetiology occurring uniquely in male BXSB mice during the course of their SLE may be responsible for the enhanced expression of serum gp70 antigen, because of its nature as an acute phase reactant and (2) enhanced expression of gp70 antigen is associated with increased formation of anti-gp70 antibodies and exacerbation of lupus nephritis in male BXSB mice.