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Helicobacter pylori targets dendritic cells to induce immune tolerance, promote persistence and confer protection against allergic asthma


Oertli, Mathias; Müller, Anne (2012). Helicobacter pylori targets dendritic cells to induce immune tolerance, promote persistence and confer protection against allergic asthma. Gut Microbes, 3(6):566-571.

Abstract

The bacterial pathogen Helicobacter pylori is predominantly known for its tight association with peptic ulcer disease and gastric cancer. However, recent evidence suggests that chronic infection with H. pylori may also be beneficial to the host by conferring protection against allergies, asthma and inflammatory bowel diseases. The protective effects of H. pylori depend on highly suppressive regulatory T-cells. In this addendum, we summarize results showing that H. pylori infection efficiently re-programs dendritic cells (DCs) toward a tolerance-promoting phenotype; their "tolerogenic" activity requires inflammasome activation and the secretion of interleukin-18. H. pylori-experienced DCs fail to induce T-cell effector functions, but efficiently induce FoxP3 expression in naive T-cells in vitro and in vivo. The experimental depletion of DCs breaks tolerance and results in improved infection control, but also in aggravated T-cell-driven immunopathology. In summary, we propose that H. pylori evades adaptive immune responses by re-programming DCs in favor of tolerance over immunity.

Abstract

The bacterial pathogen Helicobacter pylori is predominantly known for its tight association with peptic ulcer disease and gastric cancer. However, recent evidence suggests that chronic infection with H. pylori may also be beneficial to the host by conferring protection against allergies, asthma and inflammatory bowel diseases. The protective effects of H. pylori depend on highly suppressive regulatory T-cells. In this addendum, we summarize results showing that H. pylori infection efficiently re-programs dendritic cells (DCs) toward a tolerance-promoting phenotype; their "tolerogenic" activity requires inflammasome activation and the secretion of interleukin-18. H. pylori-experienced DCs fail to induce T-cell effector functions, but efficiently induce FoxP3 expression in naive T-cells in vitro and in vivo. The experimental depletion of DCs breaks tolerance and results in improved infection control, but also in aggravated T-cell-driven immunopathology. In summary, we propose that H. pylori evades adaptive immune responses by re-programming DCs in favor of tolerance over immunity.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Molecular Cancer Research
07 Faculty of Science > Institute of Molecular Cancer Research
Dewey Decimal Classification:570 Life sciences; biology
Language:English
Date:2012
Deposited On:24 Sep 2012 13:15
Last Modified:05 Apr 2016 15:56
Publisher:Landes Bioscience
ISSN:1949-0984
Publisher DOI:https://doi.org/10.4161/gmic.21750
PubMed ID:22895083

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