[Immunological and non-immunological mechanisms of tubulo-interstitial nephropathies].
Studies in experimental models and human cases provide compelling evidence for immune mechanisms of tubulo-interstitial nephropathy (TIN) or tubulo-interstitial nephritis. Analogous to immune-mediated glomerular injuries, anti-tubular basement membrane antibodies, immune complex deposition, antibodies with cell-surface antigens and cell-mediated reactions may contribute to the initiation and progression of TIN. Recent studies further indicate that local expression of cytokines, growth factors and adhesion molecules along with activation of tubular epithelial cells and fibroblasts participates in the inflammation and fibrogenesis in the renal interstitium. This process may also occur secondarily to primary glomerulonephritis, in which the tubulo-interstitial injury is suggested to be closely associated with the decline in renal function.
Yoshioka
K
K
Department of Pediatrics, Kinki University School of Medicine.
D000818:Animals; D000936:Antigen-Antibody Complex; D001323:Autoantibodies / Q000276:immunology; D001485:Basement Membrane / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D005347:Fibroblasts; D006133:Growth Substances / Q000502:physiology; D006801:Humans; D007111:Immunity, Cellular; D007684:Kidney Tubules / Q000276:immunology; D009395:Nephritis, Interstitial / Q000209:etiology* / Q000276:immunology
D000936:Antigen-Antibody Complex; D001323:Autoantibodies; D015815:Cell Adhesion Molecules; D016207:Cytokines; D006133:Growth Substances