幽门螺杆菌逃避宿主免疫应答的机制  

Mechanism of Helicobacter pylori Evasion of Host Immune Response

作　　者：周妍[1] 姚玉峰[1] 郭晓奎[1] 

机构地区：[1]上海交通大学医学院病原生物学教研室,200025

出　　处：《胃肠病学》2007年第10期628-630,共3页Chinese Journal of Gastroenterology

摘　　要：幽门螺杆菌(H.pylori)感染后,宿主会产生强烈的炎症反应和免疫反应,表现为胃黏膜中性粒细胞、淋巴细胞以及单核巨噬细胞大量浸润。在这些不同的细胞类型中,T淋巴细胞对清除H.pylori感染起最为重要的作用。以往的研究结果提出了H.pylori与宿主免疫对抗的可能机制,并发现H.pylori在宿主体内持续定植可能与空泡形成细胞毒素A(VacA)和脂多糖(LPS)有关。本文就VacA和LPS对免疫应答,特别是对T淋巴细胞免疫应答的影响作一综述,阐述H.pylori逃避宿主免疫应答的相关因素,以期对今后H.pylori的预防和治疗提供线索。Inflammatory reaction and host immune response caused by Helicobacter priori （H. pylori ） are characterized by dense infiltration of the mucosa with neutrophils, lymphocytes, and monocytes/macrophages. Among these cells, T-lymphocytes play the most crucial role in eliminating bacteria. Previous studies elucidated that the possible mechanisms on how H. pylori interfered with the human immune response and found that vacuolating cytotoxin A （VacA） and lipopolysaccharide （LPS） were probably responsible for the persistence of the bacterial infection. This review article introduced the effects of VacA and LPS on host immune response, especially T-lymphocytes, and elucidated the factors involved in H. pylori evading host immune responses, which might provide novel strategies for prevention and treatment of H. priori infection.

关 键 词：螺杆菌 幽门 免疫逃逸 T淋巴细胞 空泡毒素 脂多糖类 

分 类 号：R392[医药卫生—免疫学] R378[医药卫生—基础医学]