AUTOANTIBODIES TO RIBOSOMAL P-ANTIGEN WITH IMMUNE-COMPLEX GLOMERULONEPHRITIS IN SJL MICE TREATED WITH PRISTANE

BALB/c ByJ mice develop a lupus-like syndrome characterized by anti-nR NP/Sm and Su autoantibodies and immune complex glomerulonephritis afte r a single i.p. pristane injection, In contrast, mercuric chloride ind uces anti-fibrillarin Abs only in SJL and other H-2(s) mice, and not i n BALB/c (H-2(d)) mice, In the present study, the specificities of aut oantibodies induced by pristane and HgCl2 were compared in SJL and BAL B/c mice to examine whether these strains are ''programmed'' to make d ifferent sets of autoantibodies in response to nonspecific immune stim ulation, Unexpectedly, the predominant autoantibodies induced by prist ane in SJL mice were neither those characteristic of HgCl2-treated SJL mice nor those associated with pristane-induced disease in BALB/c mic e but, rather, anti-ribosomal P, another lupus-related specificity, Th e autoantibodies were strongly reactive with the C-terminal 22 amino a cids of the ribosomal P2 protein, indicating that they exhibited simil ar fine specificities to anti-P Abs in human SLE and MRL/lpr mice, Lik e BALB/c mice, pristane-treated SJL mice developed severe glomerulonep hritis characterized by proteinuria, mesangial proliferation, and glom erular immune complex deposits, This is the first evidence that the in duction of a lupus-like syndrome by pristane is not restricted to BALB /c mice. The predominance of anti-P Abs in SJL mice contrasts sharply with the predominance of anti-nRNP/Sm and Su, in pristane-treated BALB /c mice, even though the renal lesions were similar in both strains, T he data suggest that H-2(s) does not program mice to produce anti-fibr illarin Abs in response to nonspecific immune stimulation, arguing tha t autoantibody induction by pristane involves Ag-specific mechanisms.