Deficient interleukin‐2 responsiveness of T lymphocytes from patients with primary biliary cirrhosis
Deficient interleukin‐2 responsiveness of T lymphocytes from patients with primary biliary cirrhosis
复制标题
原发性胆汁性肝硬化患者 T 淋巴细胞白细胞介素 2 反应性缺陷
作者：
José Luis Menéndez;J. Girón;L. Manzano;Aurelio Garrido;L. Abreu;A. Albillos;A. Durántez;M. Alvarez‐Mon
越来越多的证据表明原发性胆汁性肝硬化与免疫系统的改变有关。尽管病因尚不清楚，但有人认为原发性胆汁性肝硬化患者的免疫系统参与了其疾病的发病机制。我们研究了原发性胆汁性肝硬化患者的 T 细胞功能，发现植物血凝素诱导的 T 细胞有丝分裂存在缺陷。同样，尽管佛波酯（12-O-十四油佛波醇-13-乙酸酯）加离子载体（离子霉素）刺激诱导的 DNA 合成正常，但它们对 CD3 单克隆抗体的胚细胞反应也受到抑制。这些改变不能归因于白介素-2 合成的减少或细胞激活后白细胞介素-2 受体的表达缺陷。此外，即使在存在饱和浓度的外源性白介素-2 的情况下，也观察到 T 淋巴细胞的这种有缺陷的增殖反应。这些结果证明原发性胆汁性肝硬化患者的 T 淋巴细胞中存在白细胞介素 2 依赖性途径缺陷。 （肝病学 1992；16：931–936。）
There is increasing evidence that primary biliary cirrhosis is associated with an alteration of the immune system. Although the cause remains unknown, it has been suggested that the immune system of patients with primary biliary cirrhosis is involved in the pathogenesis of their disease. We have investigated the T‐cell function in patients with primary biliary cirrhosis and have found defective phytohemagglutinin‐induced T‐cell mitogenesis. Likewise, their blastogenic response to CD3 monoclonal antibody was also depressed, although the DNA synthesis induced by stimulation with phorbol esters (12‐O‐tetradecanoilphorbol‐13‐acetate) plus ionophore (ionomycin) was normal. These alterations could not be ascribed either to a decreased synthesis of interleukin‐2 or to a defective expression of interleukin‐2 receptor after cellular activation. Moreover, this defective proliferative response of T lymphocytes was observed even in the presence of saturating concentrations of exogenous interleukin‐2. These results represent evidence of the deficiency in the interleukin‐2—dependent pathway found in T lymphocytes from patients with primary biliary cirrhosis. (HEPATOLOGY 1992;16:931–936.)