In studying the processes that contribute to the increased severity of lupus-like disease upon loss of both GILZ and Lyn, we found that while autoantibody production overall was not significantly altered by the loss of GILZ, anti-dsDNA antibodies that are strongly associated with nephritis in human SLE were significantly increased in older double-deficient mouse strain compared to Lyn-/-. Here, TSC22D3 is linked to nephritis.