NZB/NZW F1 mice (B/W) spontaneously develop an autoimmune disease resembling human systemic lupus erythematosus (SLE) (1, 2). This includes LE cell and anti-nuclear factor formation, severe glomerulonephritis, and uremia. The serologic and histologic abnormalities appear earlier in the female B/W mice who generally die of nephritis by 10 months of age. The renal disease is considered a soluble immune complex type of nephritis (3). DNA, anti-DNA antibodies and complement have been demonstrated in the glomeruli of these mice (3) as well as in patients with SLE (4). Previous studies demonstrating serum anti-DNA antibodies in B/W mice have employed the techniques of immunofluorescence (3, 5), immuno-diffusion and complement fixation (3). These indirect methods are limited by variable patterns of fluorescent staining, non-precipitating antibody and anti-complementary activity. Recently a sensitive assay measuring the direct binding of radioactive DNA by immunoglobulin has been described for humans with SLE (6, 7).