T lymphocyte participation in antibody-induced experimental glomerulonephritis.
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.
D000818:Animals; D000906:Antibodies / Q000276:immunology; D001485:Basement Membrane / Q000276:immunology; D002465:Cell Movement; D003524:Cyclosporins / Q000494:pharmacology; D005921:Glomerulonephritis / Q000276:immunology* / Q000473:pathology; D007111:Immunity, Cellular; D007678:Kidney Glomerulus / Q000648:ultrastructure; D008264:Macrophages / Q000473:pathology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000473:pathology*
D000906:Antibodies; D003524:Cyclosporins