Mayet W J, Press A G, Hermann E, Moll R, Manns M, Ewe K, Meyer zum Büschenfelde K H
Institute of Pathology, University of Mainz, FRG.
Eur J Clin Invest. 1990 Oct;20(5):516-24. doi: 10.1111/j.1365-2362.1990.tb01895.x.
The immunologic basis of inflammatory bowel disease has been the focus of interest of a series of studies on Crohn's disease and the process of immune sensitization at the gastrointestinal mucosal level is functionally poorly understood. To date only few contradictory reports concerning the incidence of autoantibodies in patients with this disease exist. The aim of this study was to investigate the sera drawn from 60 patients suffering from biopsy-proven Crohn's disease to evaluate the prevalence of autoantibodies against nuclear antigens and cytoskeletal proteins. Using standard methods, no anti-nuclear antibodies or antibodies to extractable nuclear antigens could be detected. All sera were also negative for antibodies to double-stranded DNA, anti-mitochondrial antibodies, and antibodies to gastric parietal cells. Using sensitive enzyme-linke immunosorbent assays with purified antigens and Western blotting with cytoskeletal proteins of human intestinal cells, the following antibodies could be demonstrated: cytokeratin 18 autoantibodies (IgG 20.0%; IgM 6.7%; IgA 13.3%), actin antibodies (IgG 36.7%; IgM 48.3%, IgA 26.7%), desmin antibodies (IgG 6.7%; IgM 15.08%; IgA 5.0%), vimentin antibodies (IgG 3.3%; IgM 16.7%; IgA 10.0%) and tropomyosin antibodies (IgG 3.3%; IgM 3.3%, IgA 5.0%). Statistically significant correlations could be found for levels of cytokeratin 18 antibodies (IgM-type) and the BEST index of activity, and for levels of desmin antibodies (IgM-type) and the van HEES index of activity. Highest levels could be measured for actin antibodies (IgG-type) in patients with isolated disease manifestation in the colon. The mechanism of induction of autoantibodies against cytoskeletal components in Crohn's disease still remains obscure. Unmasking of hidden antigens after cell injury during the inflammatory process of disease might lead to sensitization and antibody production. The pattern of antibodies in patients with Crohn's disease seems to be different compared with that of connective tissue diseases.
炎症性肠病的免疫基础一直是一系列关于克罗恩病研究的关注焦点,而胃肠道黏膜水平的免疫致敏过程在功能上仍未得到充分理解。迄今为止,关于该疾病患者自身抗体发生率的报道很少且相互矛盾。本研究的目的是检测60例经活检证实为克罗恩病患者的血清,以评估抗核抗原和细胞骨架蛋白自身抗体的流行情况。采用标准方法,未检测到抗核抗体或可提取核抗原的抗体。所有血清的双链DNA抗体、抗线粒体抗体和胃壁细胞抗体也均为阴性。使用纯化抗原的敏感酶联免疫吸附测定法以及人肠道细胞骨架蛋白的蛋白质印迹法,可检测到以下抗体:细胞角蛋白18自身抗体(IgG 20.0%;IgM 6.7%;IgA 13.3%)、肌动蛋白抗体(IgG 36.7%;IgM 48.3%,IgA 26.7%)、结蛋白抗体(IgG 6.7%;IgM 15.08%;IgA 5.0%)、波形蛋白抗体(IgG 3.3%;IgM 16.7%;IgA 10.0%)和平滑肌肌动蛋白抗体(IgG 3.3%;IgM 3.3%,IgA 5.0%)。细胞角蛋白18抗体(IgM型)水平与BEST活动指数之间以及结蛋白抗体(IgM型)水平与van HEES活动指数之间存在统计学上的显著相关性。在结肠孤立性疾病表现的患者中,肌动蛋白抗体(IgG型)水平最高。克罗恩病中针对细胞骨架成分的自身抗体诱导机制仍不清楚。疾病炎症过程中细胞损伤后隐藏抗原的暴露可能导致致敏和抗体产生。克罗恩病患者的抗体模式似乎与结缔组织疾病不同。