Macrophage accumulation is a feature of some aggressive forms of human and experimental glomerulonephritis (GN). Both antibody Fc components and T cells may cause macrophage accumulation; however, there has been no previous demonstration of T cells at the site of injury in GN, although some indirect evidence of their possible participation has been reported. Specific monoclonal anti-rat T lymphocyte antibodies W3/13, W3/25, and Ox8 were used to demonstrate T cells within the glomeruli of rats with an augmented autologous anti-GBM GN, by indirect immunofluorescence. The injury in this model has been shown to be mediated by macrophages. The T cell infiltrate consisted mainly of T helper cells, was maximal 24 hr after induction of the disease and clearly preceded the peak influx of macrophages and glomerular damage. Suppression of T cell function using cyclosporin prevented T cell accumulation and the subsequent macrophage-induced injury. Glomerular T cells were not seen in passively induced GN. These studies support a role for cell-mediated immunity in attracting macrophages and initiating injury in experimental anti-GBM antibody-induced GN.