Interferon- (cid:1) is required for lupus nephritis in mice treated [2] and can have a direct pathogenic role in glomerulo- with the hydrocarbon oil pristane. nephritis [3, 4]. Nephritis and autoantibodies characteris- Background. Although the precise mechanisms leading to tic of systemic lupus erythematosus (SLE) also occur lupus nephritis remain obscure, both T H 1 and T H 2 cytokines spontaneously in certain strains of mice, such as NZB/W have been implicated. The present study examined the roles of (F1) and MRL/ lpr [4]. Murine lupus models facilitate interleukin (IL)-4 and interferon- (cid:1) (IFN- (cid:1) ) in a novel inducible form of lupus that develops in non-autoimmune mice treated studies of the relationship between autoantibody forma- with the hydrocarbon oil pristane. tion and end organ damage [4–6]. Like SLE, murine Methods. BALB/c IL-4 or IFN- (cid:1) deficient mice (IL-4 (cid:2) / (cid:2) , lupus has a strong genetic component [7]. However, IFN (cid:1) (cid:2) / (cid:2) ) and wild type controls ( (cid:3) / (cid:3) ) received either pris-there are differences between murine and human analyzed for anti-DNA/chromatin, anti-RNP/Sm, and total immunoglobulin levels. Proteinuria and kid-found neys were examined by direct immunofluorescence and lupus including both clinical Conclusions. IFN- (cid:1) is essential for the induction of nephri-features (arthritis, serositis, glomerular hypercellularity, tis and anti-DNA/chromatin following pristane exposure in glomerular IC deposition, proteinuria) and the autoanti- BALB/c mice, suggesting that genetic or environmental factors influencing T H 1-T H 2 balance could be an important deter-body profile -nRNP/Sm, -chromatin, minant of renal disease in lupus. Glomerular staining was evaluate the effects of T H 1 versus T H 2 cytokines in pris-graded by intensity (0 (cid:7) no staining, 4 (cid:3) (cid:7) maximum tane-induced lupus. We show that the proinflammatory intensity staining) and pattern (predominantly mesangial cytokine IFN- (cid:1) plays a key role in the development of vs. capillary plus mesangial). Background was defined both autoantibodies and nephritis in pristane-treated mice.