Lymphocytes in the human gastric mucosa during Helicobacter pylori have a T helper cell 1 phenotype
Lymphocytes in the human gastric mucosa during Helicobacter pylori have a T helper cell 1 phenotype
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DOI：
10.1016/s0016-5085(98)70531-1
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发表时间：
1998-03-01
期刊：
影响因子：
29.4
通讯作者：
Ernst, PB
中科院分区：
文献类型：
--
作者：
Bamford, KB;Fan, XJ;Ernst, PB
背景与目的：研究表明，幽门螺杆菌感染时胃T细胞增多。本研究的目的是研究幽门螺杆菌存在或不存在时人胃T细胞的反应。方法：采用免疫组织化学方法或分离后检测T细胞表面抗原，用流式细胞仪检测T细胞表面抗原和胞浆细胞因子。结果：在幽门螺杆菌感染过程中，CD4(+)和CD8(+)T细胞原位增加。新鲜分离的胃T细胞在短暂刺激后表达胞浆干扰素-γ和白介素2。同时四色流式细胞术检测CD8(+)和CD4(+)T细胞均表达干扰素-γ。由于CD30刺激有利于IL-5和Th2细胞的诱导，因此检测了胃和结肠T细胞CD30的表达。与肠道中发现Th2细胞的观点一致，CD30在结肠固有层中明显存在，但在胃中几乎没有。此外，新鲜分离的胃T细胞产生的IL-4很少，几乎没有IL-5或肿瘤坏死因子β。结论：胃T细胞与Th1型细胞相似，这可能是它们不能诱导幽门螺杆菌免疫的原因，也是它们在胃病发病中起作用的原因。
Background & Aims: Studies have shown that gastric T cells are increased during Helicobacter pylori infection. The purpose of this study was to characterize the human gastric T-cell responses in the presence or absence of H. pylori. Methods: T-cell surface antigens were examined by immunohistochemistry or after isolation for evaluation of surface antigens and cytoplasmic cytokines using flow cytometry. Results: CD4(+) and CD8(+) T cells were increased in situ during infection with H. pylori. Freshly isolated gastric T cells expressed cytoplasmic interferon gamma (IFN-gamma) and interleukin (IL)-2 after a brief stimulation. Simultaneous four-color flow cytometry demonstrated that both CD8(+) and CD4(+) T cells expressed IFN-gamma. Because stimulation through CD30 favors the induction of IL-5 and Th2 cells, gastric and colonic T cells were examined for CD30 expression. Consistent with the notion that Th2 cells are found in the intestine, CD30 was evident throughout the lamina propria of the colon but was virtually absent in the stomach. Furthermore, freshly isolated gastric T cells produced little IL-4 and virtually no IL-5 or tumor necrosis factor beta. Conclusions: These observations show that gastric T cells resemble the Th1 type, which may explain their failure to induce immunity to H. pylori and their ability to contribute to the pathogenesis of gastric disease.