4.6 Article

Immune evasion strategies used by Helicobacter pylori

期刊

WORLD JOURNAL OF GASTROENTEROLOGY
卷 20, 期 36, 页码 12753-12766

出版社

BAISHIDENG PUBLISHING GROUP INC
DOI: 10.3748/wjg.v20.i36.12753

关键词

Helicobacter pylori; Immune response; Pattern recognition receptors; Phagocytes; T cells; Antigen presenting cells; Gastric epithelial cells; Vacuolating cytotoxin; T4SS

资金

  1. National Institutes of Health [K22AI68712, R56DK090090-01]
  2. American Gastroenterological Association Research Scholar Award, NIH [1U54RR02614]
  3. University of Texas Medical Branch Clinical and Translational Sciences Award
  4. American cancer society [RSG-10-159-01-LIB]
  5. NIH [8UL1TR000041]
  6. University of New Mexico clinical and Translational Science Center
  7. Sealy Centre for Vaccine Development Pre-doctoral fellowship
  8. McLaughlin Pre-doctoral Fellowship, UTMB

向作者/读者索取更多资源

Helicobacter pylori (H. pylori) is perhaps the most ubiquitous and successful human pathogen, since it colonizes the stomach of more than half of humankind. Infection with this bacterium is commonly acquired during childhood. Once infected, people carry the bacteria for decades or even for life, if not treated. Persistent infection with this pathogen causes gastritis, peptic ulcer disease and is also strongly associated with the development of gastric cancer. Despite induction of innate and adaptive immune responses in the infected individual, the host is unable to clear the bacteria. One widely accepted hallmark of H. pylori is that it successfully and stealthily evades host defense mechanisms. Though the gastric mucosa is well protected against infection, H. pylori is able to reside under the mucus, attach to gastric epithelial cells and cause persistent infection by evading immune responses mediated by host. In this review, we discuss how H. pylori avoids innate and acquired immune response elements, uses gastric epithelial cells as mediators to manipulate host T cell responses and uses virulence factors to avoid adaptive immune responses by T cells to establish a persistent infection. We also discuss in this review how the genetic diversity of this pathogen helps for its survival. (C) 2014 Baishideng Publishing Group Inc. All rights reserved.

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