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急性酒精性肝炎中针对65 kDa热休克蛋白的循环IgA抗体

Circulating IgA antibody against a 65 kDa heat shock protein in acute alcoholic hepatitis.

作者信息

Winrow V R, Bird G L, Koskinas J, Blake D R, Williams R, Alexander G J

机构信息

ARC Bone and Joint Research Unit, London Hospital Medical College, UK.

出版信息

J Hepatol. 1994 Mar;20(3):359-63. doi: 10.1016/s0168-8278(94)80008-1.

Abstract

Heat shock proteins are known to be immunogenic in a number of diverse conditions and can be induced by hypoxia, tumour necrosis factor and alcohol--all potential triggers in patients with acute alcoholic hepatitis. In the present study, sera from 23 patients with acute alcoholic hepatitis, 18 liver disease controls, ten patients with inactive alcoholic liver disease and six alcoholics without liver damage were screened for the antibody to a 65 kDa heat shock protein using an ELISA technique. IgA antibody was found to be closely associated with alcoholic hepatitis; 20/23 patients were seropositive compared to 5/18 liver disease controls and 4/10 with inactive alcoholic cirrhosis. IgM and IgG antibodies to the 65 kDa heat shock protein were less closely associated with alcoholic hepatitis and were positive in nine and eight of the 23 patients, respectively, compared with six and seven of 18 liver disease controls. Neither antibody was detected in alcoholics without liver damage or normal controls. These data indicate that an IgA immune mediated response to the 65 kDa heat shock protein is characteristic of patients with acute alcoholic hepatitis and may be one mechanism underlying observed persistence of liver damage after cessation of alcohol consumption.

摘要

已知热休克蛋白在多种不同情况下具有免疫原性,并且可由缺氧、肿瘤坏死因子和酒精诱导产生,而这些都是急性酒精性肝炎患者的潜在触发因素。在本研究中,采用酶联免疫吸附测定(ELISA)技术,对23例急性酒精性肝炎患者、18例肝病对照者、10例非活动性酒精性肝病患者和6例无肝损伤的酗酒者的血清进行了针对一种65 kDa热休克蛋白抗体的筛查。发现IgA抗体与酒精性肝炎密切相关;23例患者中有20例血清学呈阳性,而肝病对照者中18例有5例呈阳性,非活动性酒精性肝硬化患者中10例有4例呈阳性。针对65 kDa热休克蛋白的IgM和IgG抗体与酒精性肝炎的相关性较弱,23例患者中分别有9例和8例呈阳性,而18例肝病对照者中分别有6例和7例呈阳性。在无肝损伤的酗酒者或正常对照者中均未检测到这两种抗体。这些数据表明,针对65 kDa热休克蛋白的IgA免疫介导反应是急性酒精性肝炎患者的特征,可能是戒酒之后观察到的肝损伤持续存在的潜在机制之一。

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