Seven-month-old NZB/W F1 mice were inoculated with 5 X 10(7) NZW spleen cells. The mice so treated showed a clear fall of anti-double-stranded (ds) DNA antibody titers accompanied by a decrease in blood urea nitrogen (BUN) concentration. Mice so treated showed markedly increased survival times (more than 17 months) compared with untreated controls (mean +/- SD 8.38 +/- 0.75 months). A cell fractionation study suggested that T cells among NZW spleen cells play a major role. Recipients of the unfractionated or the T-cell fraction of NZW spleen cells had histologically less glomerulonephritis than untreated control NZB/W F1 mice. NZW B-cell transfer to NZB/W F1 mice had no effect. Serum obtained from NZB/W F1 mice receiving NZW spleen cells 10 days previously (graft-vs-host (GVHR) serum) was injected into 8-month-old NZB/W F1 mice. A clear fall in anti-ds DNA antibody titers and inhibition of age-associated sharp increases in BUN were observed. The mean life span of these mice (10.50 +/- 0.58 months) was significantly longer than that of untreated controls (8.69 +/- 0.38 months). GVHR serum had the ability to suppress anti-ds DNA antibody formation by NZB/W F1 spleen cells in vitro. Allogeneic GVHR serum prepared in C57B1/6 X DBA/2 (BDF1) mice by transferring C57B1/6 spleen cells was also effective in suppressing anti-ds DNA antibody formation in vitro.