Cochrane A M, Tsantoulos D C, Moussouros A, McFarlane I G, Eddleston A L, Williams R
Br Med J. 1976 Jul 31;2(6030):276-8. doi: 10.1136/bmj.2.6030.276.
Sensitisation to a renal tubular antigen, Tamm-Horsfall glycoprotein, has been shown to be common in patients with renal tubular acidosis complicating autoimmune liver disease, and it has been suggested that this immune reaction, by damaging renal tubular cells, might be responsible for the acidification defect. The lymphocytes from 10 out of 13 patients with chronic active hepatitis or primary biliary cirrhosis and an associated renal tubular acidosis were shown to be cytotoxic for a kidney cell line known to secrete Tamm-Horsfall glycoprotein. The cytotoxic reaction was blocked by this antigen, but not by two other proteins, indicating that sensitisation to the renal glycoprotein was the likely cause of the target cell damage. Significant reduction in cytotoxicity after the addition of aggregated IgG suggested that the reaction was of the antibody-dependent cell-mediated type. These results, together with the finding of antigenic material in the surface membrane of liver cells that cross reacts immunologically with Tamm-Horsfall glycoprotein, provide an explanation for the association between chronic liver disease and renal tubular dysfunction.
在合并自身免疫性肝病的肾小管酸中毒患者中，对肾小管抗原（Tamm-Horsfall糖蛋白）致敏很常见，有人认为这种免疫反应通过损伤肾小管细胞，可能是酸化缺陷的原因。13例慢性活动性肝炎或原发性胆汁性肝硬化合并肾小管酸中毒患者中，有10例患者的淋巴细胞对已知分泌Tamm-Horsfall糖蛋白的肾细胞系具有细胞毒性。这种细胞毒性反应被该抗原阻断，但未被其他两种蛋白质阻断，表明对肾糖蛋白致敏可能是靶细胞损伤的原因。加入聚集的IgG后细胞毒性显著降低，提示该反应为抗体依赖性细胞介导型。这些结果，连同在肝细胞表面膜中发现与Tamm-Horsfall糖蛋白发生免疫交叉反应的抗原物质，为慢性肝病与肾小管功能障碍之间的关联提供了解释。
