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 mizoribine, a new immunosuppressive agent. The ddY mice were treated with a low (0.05 mg/ml) or a high (0.1 mg/ml) dose of mizoribine for 35 weeks. Flow cytometry analysis showed that there was a marked decrease in the number of B cells and IgA-bearing B cells. In immunofluorescence, the deposition of IgA in the glomerular mesangial areas and capillary walls of the high-dose mizoribine-treated ddY mice was markedly decreased as compared with that of control ddY mice receiving drinking water. The glomerular mesangial expansion in the high-dose mizoribine-treated ddY mice was milder than that found in the control ddY mice. In 45-week-old ddY mice, the average number of intraglomerular cells in the high-dose and low-dose mizoribine-treated ddY mice was slightly lower than that in drinking water treated ddY mice. The levels of urinary protein excretion in the high-dose mizoribine-treated ddY mice were also lower than those in the low-dose mizoribine-treated or drinking water treated ddY mice. It appears that treatment of mizoribine might influence the proliferation of B cells, especially IgA-bearing B cells, and improve the glomerular IgA deposition and glomerular expansion in early-stage IgA nephropathy of ddY mice.