Immunopathogenetic mechanisms in renal disease.
This review deals with various immunopathogenetic mechanisms of renal diseases. Although immune-complex nephritis was long thought to be the result of deposition of circulating immune complexes, recent studies have revealed the importance of in situ formation. In experimental Heymann nephritis, an antigen (gp 330) has been localized on glomerular epithelial cells, and antibodies reactive with gp 330 have been eluted from glomeruli; deposits appear to result from shedding of complexes from the podocyte surface into the basement membrane. In human disease, it seems likely that mesangial and subendothelial deposits most often result from deposition of circulating immune complexes, whereas subepithelial deposits are formed mainly in situ. Cell-mediated immune mechanisms are capable of producing glomerular injury, as shown in experimental models. In humans, Wegener's granulomatosis and idiopathic crescentic glomerulonephritis may involve such mechanisms. In certain forms of experimental and human tubulointerstitial nephritis, cell-mediated immunity also seems to play an important role.
D000818:Animals; D000936:Antigen-Antibody Complex / Q000276:immunology; D001327:Autoimmune Diseases / Q000276:immunology; D005921:Glomerulonephritis / Q000276:immunology; D006801:Humans; D007105:Immune Complex Diseases / Q000276:immunology; D007111:Immunity, Cellular; D007674:Kidney Diseases / Q000276:immunology*; D009393:Nephritis / Q000276:immunology; D009395:Nephritis, Interstitial / Q000276:immunology
D000936:Antigen-Antibody Complex