Lymphocyte cytotoxicity for kidney cells in renal tubular acidosis of autoimmune liver disease.
Lymphocyte cytotoxicity for kidney cells in renal tubular acidosis of autoimmune liver disease.
复制标题
自身免疫性肝病肾小管酸中毒中淋巴细胞对肾细胞的细胞毒性。
作者：
A. Cochrane;D. C. Tsantoulos;A. Moussouros;I. Mcfarlane;A. Eddleston;R. Williams
对肾小管抗原Tamm-Horsfall糖蛋白的敏感性在自身免疫性肝病合并肾小管酸中毒的患者中很常见，有人认为这种免疫反应通过破坏肾小管细胞，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变和伴发肾小管性酸中毒的10例患者的淋巴细胞对一种已知分泌Tamm-Horsfall糖蛋白的肾细胞系具有细胞毒作用。这种细胞毒性反应可被该抗原阻断，但不能被另外两种蛋白质阻断，这表明对肾糖蛋白的敏感性可能是靶细胞损伤的原因。加入聚集的免疫球蛋白后，细胞毒性显著降低，提示该反应是抗体依赖的细胞介导型反应。这些结果，加上在肝细胞表膜上与Tamm-Horsfall糖蛋白发生免疫交叉反应的抗原物质的发现，为慢性肝病和肾小管功能障碍之间的联系提供了解释。
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.