Immunofluorescence studies were performed to determine whether the expression of intercellular adhesion molecule 1 (ICAM-1) in ddY mice, a model for IgA nephropathy (Berger’s disease), is influenced by treatment with a rat monoclonal antibody to murine CD4 molecules. The ddY mice were initially treated with intravenous injections, followed by weekly intraperitoneal injections of monoclonal antibody CD4. Using immunofluorescence, the mean intensity of IgA deposits in renal glomerular mesangial areas and capillary walls of the treated ddY mice was significantly lower than that in saline-treated control ddY mice of comparable ages. Marked expression of ICAM-1 was observed in glomerular capillary walls and mesangial areas in both control and treated ddY mice aged 40 and 70 weeks. The glomerular mesangial expansion in the treated ddY mice was milder than that found in the control ddY mice. No significant difference in glomerular cell proliferation between the treated and control ddY mice was observed. Although the infiltration of CD4+ T cells in glomeruli was slightly decreased after the treatment, that of CD8+ T cells and macrophages/monocytes was marked in both control and treated ddY mice aged 40 and 70 weeks. Thus, it appears that CD4+ T cells modulate the amount of IgA deposits in glomeruli, and other factors may be involved in the expression of ICAM-1 in glomeruli of IgA nephropathy in ddY mic