Previous studies have shown that deletion of IL-23R in B6/lpr and MRL/lpr mice reduced DN T, IFNγ- and IL-17- producing cells, suppressed anti-dsDNA autoantibodies and total IgG production, reduced immune complex deposition, and ameliorated lupus nephritis in the lpr lupus mice (44, 45). The gene discussed is IL17A; the disease is lupus nephritis.