H. pylori exploits and manipulates innate and adaptive immune cell signaling pathways to establish persistent infection

被引:62
作者
Mueller, Anne [1 ]
Oertli, Mathias [1 ]
Arnold, Isabelle C. [1 ,2 ]
机构
[1] Univ Zurich, Inst Mol Canc Res, Zurich, Switzerland
[2] Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England
来源
CELL COMMUNICATION AND SIGNALING | 2011年 / 9卷
基金
瑞士国家科学基金会;
关键词
immune evasion; innate immune signaling; immunomodulation; persistent infection; REGULATORY T-CELLS; HELICOBACTER-PYLORI; VACUOLATING TOXIN; EPITHELIAL-CELLS; BACTERIAL PEPTIDOGLYCAN; ANTIBODIES IMPAIR; NOD1; ACTIVATION; RESPONSES; ASTHMA;
D O I
10.1186/1478-811X-9-25
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Persistent infection with the gastric bacterial pathogen Helicobacter pylori causes gastritis and predisposes carriers to a high gastric cancer risk, but has also been linked to protection from allergic, chronic inflammatory and autoimmune diseases. In the course of tens of thousands of years of co-existence with its human host, H. pylori has evolved elaborate adaptations that allow it to persist in the hostile environment of the stomach in the face of a vigorous innate and adaptive immune response. For this review, we have identified several key immune cell types and signaling pathways that appear to be preferentially targeted by the bacteria to establish and maintain persistent infection. We explore the mechanisms that allow the bacteria to avoid detection by innate immune cells via their pattern recognition receptors, to escape T-cell mediated adaptive immunity, and to reprogram the immune system towards tolerance rather than immunity. The implications of the immunomodulatory properties of the bacteria for the prevention of allergic and auto-immune diseases in chronically infected individuals are also discussed.
引用
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页数:9
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