Faller G, Kirchner T
Institute of Pathology, University of Erlangen-Nuremberg, Germany.
Microsc Res Tech. 2000 Mar 15;48(6):321-6. doi: 10.1002/(SICI)1097-0029(20000315)48:6<321::AID-JEMT2>3.0.CO;2-U.
In recent studies a significant association between H. pylori infection and antigastric autoimmunity has been reported. Antigastric autoantibodies can be found in more than 30% of infected patients. Two distinct binding patterns of these autoantibodies have been described, first at the luminal membrane of the foveolar epithelium, and second at the canaliculi membranes of the parietal cells in the body mucosa. The latter type of autoantibodies correlates with histologic and clinical parameters of gastric mucosa atrophy. The gastric H,K-ATPase, which is known to be the autoimmune target in classical autoimmune gastritis, also represents a major autoantigen in atrophic H. pylori gastritis. Molecular mimicry between H. pylori and the host does not seem to be responsible for the generation of this type of autoreactivity. The development of antigastric autoantibodies may be a relevant host factor which contributes to the final clinical outcome of chronic H. pylori gastritis.
最近的研究报告了幽门螺杆菌感染与抗胃自身免疫之间存在显著关联。在超过30%的感染患者中可发现抗胃自身抗体。已描述了这些自身抗体的两种不同结合模式，第一种位于胃小凹上皮的腔面膜，第二种位于胃体黏膜壁细胞的小管膜。后一种自身抗体类型与胃黏膜萎缩的组织学和临床参数相关。胃H，K - ATP酶是经典自身免疫性胃炎中的自身免疫靶点，也是萎缩性幽门螺杆菌胃炎的主要自身抗原。幽门螺杆菌与宿主之间的分子模拟似乎不是这种自身反应性产生的原因。抗胃自身抗体的产生可能是一个相关的宿主因素，它有助于慢性幽门螺杆菌胃炎的最终临床结局。
