Immunopathological studies were performed to determine whether the glomerular injuries in ddY mice, a model for IgA nephropathy (Berger's disease), are influenced by treatment with a rat monoclonal antibody (mAb) to murine CD4 molecules. The ddY mice were initially treated with intravenous injections, followed by weekly intraperitoneal injections of mAb CD4. Flow cytometry analysis showed that there was a marked decrease in the number of CD4+ T cells. In immunofluorescence, the mean intensity of IgA deposits in the renal glomerular mesangial areas and capillary walls of the treated ddY mice was significantly lower than that in saline-treated control mice of comparable ages. Glomerular mesangial expansion in the treated mice was milder than that found in the saline control mice. However, no significant differences in the level of serum IgA, urinary protein, and average number of intraglomerular cells between the treated and control ddY mice were observed. Thus, it appears that although CD4+ T cells control the amount of IgA deposits in glomeruli, other factors may be involved in the evolution of IgA nephropathy in ddY mice.