[Immune reactions that mediate tubulointerstitial nephritis].
Experimental autoimmune tubulointerstitial nephritis (TIN) is induced by immunization with TBM antigen and adjuvant in guinea pigs, rats, and mice. In animal models, both anti-TBM autoantibody and TBM-sensitized T cells have important roles in development of TIN. Antibodies deposited on TBM bind with complements, and these complexes induce infiltration of macrophages and leukocytes into interstitium. And, then, lymphocytes infiltrate into the inflammatory lesions. In these lesions, inter-cellular adhesion molecule-1 (ICAM-1) is expressed within peritubular endothelia and tubular epithelia. There are several subpopulations of TBM-specific T cells associated TIN. One is Helper T cells (CD8+), they induce cytotoxic T cells which is CD8 positive and have cytotoxic activity against tubular epithelia. The function of cytotoxic T cells is downregulated by suppressor T cells.
Ueda
S
S
First Department of Medicine, Chiba University School of Medicine.
D000818:Animals; D015551:Autoimmunity; D001485:Basement Membrane / Q000276:immunology; D006168:Guinea Pigs; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000502:physiology; D007684:Kidney Tubules / Q000166:cytology / Q000276:immunology*; D051379:Mice; D009395:Nephritis, Interstitial / Q000276:immunology*; D051381:Rats; D013601:T-Lymphocytes / Q000276:immunology
D018799:Intercellular Adhesion Molecule-1