The effect of class II major histocompatibility complex expression on adherence of Helicobacter pylori and induction of apoptosis in gastric epithelial cells: a mechanism for T helper cell type 1-mediated damage.
The effect of class II major histocompatibility complex expression on adherence of Helicobacter pylori and induction of apoptosis in gastric epithelial cells: a mechanism for T helper cell type 1-mediated damage.
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DOI：
10.1084/jem.187.10.1659
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发表时间：
1998-05-18
期刊：
影响因子：
--
通讯作者：
Reyes VE
中科院分区：
文献类型：
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作者：
Fan X;Crowe SE;Behar S;Gunasena H;Ye G;Haeberle H;Van Houten N;Gourley WK;Ernst PB;Reyes VE
幽门螺杆菌感染与胃上皮损伤有关，包括细胞凋亡、溃疡和癌症。虽然细菌因素和宿主反应被认为是导致胃病的原因，但还没有发现能解释细菌如何附着并向宿主细胞发出信号以进行凋亡的受体。利用H. pylori作为“诱饵”捕获胃上皮细胞溶解膜中的受体蛋白，II类主要组织相容性复合物（MHC）分子被鉴定为可能的受体。使用与表面II类MHC分子交联的IgM抗体证实通过II类MHC分子的信号传导导致细胞凋亡的诱导。此外，H. pylori感染和细胞凋亡的诱导被识别II类MHC的抗体抑制。由于1型T辅助细胞在感染期间存在并产生干扰素（IFN）-γ，其增加II类MHC表达，因此胃上皮细胞系暴露于H. pylori中存在或不存在IFN-γ。IFN-γ可增加细菌对胃上皮细胞的粘附，并诱导胃上皮细胞凋亡。与MHC II阴性细胞系相比，H. pylori诱导的细胞凋亡表达II类MHC分子组成型或基因转染后。这些数据描述了一种新的H受体。幽门螺杆菌，并提供了一种机制，通过这种机制，细菌和宿主的反应相互作用的发病机制，胃上皮细胞损伤。
Helicobacter pylori infection is associated with gastric epithelial damage, including apoptosis, ulceration, and cancer. Although bacterial factors and the host response are believed to contribute to gastric disease, no receptor has been identified that explains how the bacteria attach and signal the host cell to undergo apoptosis. Using H. pylori as “bait” to capture receptor proteins in solubilized membranes of gastric epithelial cells, class II major histocompatibility complex (MHC) molecules were identified as a possible receptor. Signaling through class II MHC molecules leading to the induction of apoptosis was confirmed using cross-linking IgM antibodies to surface class II MHC molecules. Moreover, binding of H. pylori and the induction of apoptosis were inhibited by antibodies recognizing class II MHC. Since type 1 T helper cells are present during infection and produce interferon (IFN)-γ, which increases class II MHC expression, gastric epithelial cell lines were exposed to H. pylori in the presence or absence of IFN-γ. IFN-γ increased the attachment of the bacteria as well as the induction of apoptosis in gastric epithelial cells. In contrast to MHC II–negative cell lines, H. pylori induced apoptosis in cells expressing class II MHC molecules constitutively or after gene transfection. These data describe a novel receptor for H. pylori and provide a mechanism by which bacteria and the host response interact in the pathogenesis of gastric epithelial cell damage.