Severe glomerulonephritis was induced successfully in (B1OxDBA/2)F1(BDF1) mice by injection of parental DBA/2 lymphoid cells. The mice manifested typical ne‐phrotic syndrome dying around 10 weeks post injection. Electron microscopical examination demonstrated electron dense deposits first in the mesangial matrix, then in the subepithelium compatible with immune complex glomerulonephritis. Subendothelial deposits were not ob served. lmmunofluorescent study revealed IgG deposition in the capillary wall and IgM in the mesangium early in the process. As the lesion progressed, both IgG and IgM were present in the mesangial area and along the capillary wall. Some glomeruli showed segmental mesangiolysis, suggest ing that altered mesangial cells have a role in the develop ment of glomerular change, which together with rise in serum anti‐DNA antibody titer suggest that autoantibodies promote the glomerular lesions in this model system. Acta Pathol Jpn42: 325–332,
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