首页> 外文期刊>Hepato-gastroenterology. >Perforin and granzyme B of cytotoxic T lymphocyte mediate apoptosis irrespective of Helicobacter pylori infection: possible act as a trigger of peptic ulcer formation.
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Perforin and granzyme B of cytotoxic T lymphocyte mediate apoptosis irrespective of Helicobacter pylori infection: possible act as a trigger of peptic ulcer formation.

机译:不论幽门螺杆菌感染如何,细胞毒性T淋巴细胞的穿孔素和颗粒酶B均可介导细胞凋亡:可能是导致消化性溃疡形成的诱因。

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BACKGROUND/AIMS: The perforin/granzyme and Fas/Fas ligand pathways are two known major pathways of cytotoxic T lymphocyte-mediated apoptosis. We designed a clinical study to examine whether cytotoxic T lymphocyte-mediated apoptosis associated with peptic ulcer formation may occur via either or both of these two pathways. METHODOLOGY: Mucosal biopsy specimens were obtained endoscopically from the marginal zone of active stage gastric and duodenal ulcers in patients with or without Helicobacter pylori infection. RT-PCR, immunoblotting and immunohistochemistry were used to study the samples for the expression of apoptotic cells, perforin, granzyme B, Fas, Fas ligand and caspase 3. RESULTS: Apoptotic cells (Tunnel positive cells) appeared in the marginal zone of gastric and duodenal ulcers with and without H. pylori infection. Perforin/granzyme B and caspase 3 were expressed consistently, however Fas ligand was not. Furthermore, the immunohistochemical findings demonstrated apoptotic changes of target cells caused by perforin/granzyme B. CONCLUSIONS: These results suggest that the main pathway of cytotoxic T lymphocyte-mediated apoptosis in peptic ulcer formation is the perforin/granzyme pathway irrespective of H. pylori infection.
机译:背景/目的:穿孔素/粒酶和Fas / Fas配体途径是细胞毒性T淋巴细胞介导的细胞凋亡的两个主要途径。我们设计了一项临床研究,以检查是否可能通过这两种途径之一或全部发生与消化性溃疡形成相关的细胞毒性T淋巴细胞介导的细胞凋亡。方法:从活检阶段胃溃疡和十二指肠溃疡的边缘区域内镜下获取有或没有幽门螺杆菌感染的患者的黏膜活检标本。用RT-PCR,免疫印迹和免疫组化的方法研究了凋亡细胞,穿孔素,颗粒酶B,Fas,Fas配体和胱天蛋白酶3的表达。结果:凋亡细胞(隧道阳性细胞)出现在胃和胃的边缘区域。有和没有幽门螺杆菌感染的十二指肠溃疡。穿孔素/粒酶B和胱天蛋白酶3始终表达,但Fas配体不是。此外,免疫组织化学结果表明穿孔素/粒酶B引起靶细胞的凋亡变化。结论:这些结果表明,消化性溃疡形成中细胞毒性T淋巴细胞介导的细胞凋亡的主要途径是穿孔素/粒酶途径,而与幽门螺杆菌感染无关。 。

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