This study compares the clinical and immunopathological manifestations of spontaneous murine lupus-like syndromes in several strains of mice, including NZB × W, MRL/l, MRL/n, and BXSB. These strains develop a disease that shares many similarities with human systemic lupus erythematosus (SLE), characterized by B-cell hyperactivity, autoantibodies, circulating immune complexes (IC), abnormalities of Ig and complement, thymic atrophy, and severe IC-type glomerulonephritis with retroviral gp70 deposits. The major differences among the strains are in the amounts and specificities of autoantibodies, age of onset, and the rate of progression of the disease. The study highlights the importance of these common elements in defining SLE as a single disease across different strains, similar to the variability seen in human SLE. The findings suggest that different genetic and/or pathophysiologic factors may operate in each strain, leading to similar immunopathological outcomes. The availability of these inbred strains provides valuable resources for further research into the nature and causes of murine SLE.This study compares the clinical and immunopathological manifestations of spontaneous murine lupus-like syndromes in several strains of mice, including NZB × W, MRL/l, MRL/n, and BXSB. These strains develop a disease that shares many similarities with human systemic lupus erythematosus (SLE), characterized by B-cell hyperactivity, autoantibodies, circulating immune complexes (IC), abnormalities of Ig and complement, thymic atrophy, and severe IC-type glomerulonephritis with retroviral gp70 deposits. The major differences among the strains are in the amounts and specificities of autoantibodies, age of onset, and the rate of progression of the disease. The study highlights the importance of these common elements in defining SLE as a single disease across different strains, similar to the variability seen in human SLE. The findings suggest that different genetic and/or pathophysiologic factors may operate in each strain, leading to similar immunopathological outcomes. The availability of these inbred strains provides valuable resources for further research into the nature and causes of murine SLE.