Mercuric chloride (HgCl2) induces autoantibodies to fibrillarin (Fib) only in H-2S mice, whereas pristane induces nephritis with autoantibodies to nRNP/Sm and Su in BALB/c mice. We examined the importance of H-2 linked genes in pristane-induced autoimmunity. BALB/c ByJ (H-2), SJL/J (H-2S), and C57BI/6 (H-2b) mice were injected with pristane or HgCand sera were tested by immunoprecipitation and ELISA. As reported previously, -50% of pristane-treated BALB/c mice developed anti-Su and nRNP/Sm by 4 mo. Unexpectedly, the main specificity in pristane-treated SJL mice was antiribosomal-P (rP) (8/8 mice). Anti-Su and nRNP/Sm were rare (1/8) and antiFib was absent. In the HgCl2 group, anti-Fib, but not anti-rP, nRNP/Sm or Su was produced by SJL mice; BALB/c and B6 were negative for all. Since antirP was absent in 20 pristane-treated BALB/c, but present in all SJL mice, pristane-treated A.SW, B10.S (H-2S), and BIO (H-2b) mice were tested. Anti-rP was seen in 1/6 A.SW, 2/7 BIO, and 1/10 B6 mice, suggesting that H2 linked genes are not crucial for the induction of anti-rP. Although pristanetreated BALB/c and SJL mice exhibited different autoantibodies, both strains developed immune complex nephritis. The data suggest that pristane-induced lupus is not limited to BALB/c mice, and that autoantibody specificity is influenced by the interplay of environmental factors with background genes.
|Original language||English (US)|
|State||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology