Consistent with our observations, lupus-prone MRL-Faslpr/lpr (MRL/lpr) mice lacking ICAM-1 or lymphocyte function-associated antigen-1 showed amelioration of glomerulonephritis, which was correlated with a decrease in neutrophil accumulation in the glomeruli (34, 35). The gene discussed is ICAM1; the disease is systemic lupus erythematosus.