Ueda S
First Department of Medicine, Chiba University School of Medicine.
Nihon Rinsho. 1995 Aug;53(8):1886-93.
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.
实验性自身免疫性肾小管间质性肾炎（TIN）是通过用肾小管基底膜（TBM）抗原和佐剂免疫豚鼠、大鼠和小鼠诱导产生的。在动物模型中，抗TBM自身抗体和TBM致敏的T细胞在TIN的发展中都起着重要作用。沉积在TBM上的抗体与补体结合，这些复合物诱导巨噬细胞和白细胞浸润到间质中。然后，淋巴细胞浸润到炎症病变中。在这些病变中，细胞间黏附分子-1（ICAM-1）在肾小管周围内皮细胞和肾小管上皮细胞内表达。有几个与TIN相关的TBM特异性T细胞亚群。其中之一是辅助性T细胞（CD8+），它们诱导细胞毒性T细胞，该细胞毒性T细胞为CD8阳性且对肾小管上皮细胞具有细胞毒性活性。细胞毒性T细胞的功能被抑制性T细胞下调。
