慢性活动性肝病发病过程中自身免疫机制的干扰。

Medecine interne Pub Date : 1989-01-01
T Banciu, P Arcan, V Văcariu, N Tudose
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引用次数: 0

摘要

在两组慢性活动性肝病(CALD)患者中,研究了人肝细胞抗原在炎症过程自我延续中所起的作用。在第一组的26名患者中(14名慢性活动性肝炎患者和12名活动性肝硬化患者),在兔补体存在的情况下,将他们的血清与5.5个月大的人类胚胎肝脏培养物中的肝细胞悬浮液接触。通过微细胞毒性试验(MCT)评估肝细胞溶解,当值超过60%时被认为是阳性。以10名健康受试者和8名萎缩性胃炎患者为对照。在另外12例CALD患者(第二组)中,作者进行了通过肝脏生物穿刺获得的自体肝抗原存在的巨噬细胞迁移(IMM)和淋巴母细胞转化(LT)抑制试验。在第一组中,57.6%的患者MCT检测呈阳性,这与特定的生物形态学侵袭性和明显的免疫紊乱有关,而在对照组中,18例中有17例MCT检测呈阴性。在第二组中,自体肝细胞提取物诱导巨噬细胞迁移的明显抑制和淋巴细胞转化的显著增加。结论是在CALD患者中存在细胞毒性肝细胞抗体,以及自体肝抗原对巨噬淋巴细胞功能的刺激。在这类患者肝细胞病变的持续存在中,自身免疫机制的参与也被提出。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The interference of an autoimmune mechanism in the pathogeny of chronic active liver diseases.

The part played by the human hepatocytic antigens in the self-perpetuation of the inflammatory processes was investigated in two groups of patients with chronic active liver disease (CALD). In the 26 patients of the first group (14 with chronic active hepatitis and 12 with active cirrhosis), their serum was put in contact with a suspension of hepatocytes in a culture of liver from a 5.5 month-old human embryo, in presence of rabbit complement. The hepatocytic lysis was evaluated by the test of microcytotoxicity (MCT), considered positive at values above 60%. Ten healthy subjects and 8 patients with atrophic gastritis were used as controls. In 12 other patients with CALD (2nd group), the authors performed the test of inhibition of the macrophage migration (IMM) and that of lymphoblastic transformation (LT) in presence of an autologous liver antigen, obtained by liver biotic puncture. In the first group, the MCT test was positive in 57.6% of the patients, in correlation with a particular biomorphologic aggressivity and marked immune disturbances, while in controls it was negative in 17 of the 18 cases. In the second group, the extract of autologous hepatocytes induced a marked inhibition of the macrophage migration and a significantly increased lymphoblastic transformation. It is concluded to the existence, in the patients with CALD, of cytotoxic hepatocytic antibodies, as well as to a stimulation of the macrophagic-lymphocytic function in presence of the autologous liver antigen. The participation af an autoimmune mechanism in the perpetuation of the hepatocytic lesions in such patients is also suggested.

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