Transgenic mice develop an autoimmune disease similar to human systemic lupus erythematosus (SLE). By 4-6 months, mice develop lymphadenopathy with an unusual cell phenotype (B220+ double negative T cells) and, in most cases, splenomegaly. The phenotype occurs predominantly in females (64.5% penetrance) rather than males (20% penetrance). Additional symptoms include anti-nuclear and anti-dsDNA antibodies, increased peritoneal B-1a subpopulations, glomerulonephritis with IgG and C3 deposition, proteinuria, leukocyturia and hematuria. As mice age, they can develop skin lesions, lymphocyte infiltration to the liver, leukopenia, anemia and thrombocytopenia. Sixty three percent of female transgenics and 81.8% of male transgenics live beyond 14 months of age.

Transgenic mice express the human tumor necrosis factor receptor superfamily, member 6B (TNFRSF6B) gene under the control of the human beta actin promoter. Lupus-like symptoms occur predominantly in females and are characterized by, but not limited to, lymphadenopathy, splenomegaly, anti-nuclear and anti-dsDNA antibodies and glomerulonephritis. This mutant mouse strain may be useful in studies of systemic lupus erythematosus.

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