2013
DOI: 10.4049/jimmunol.1300524
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CagA-Dependent Downregulation of B7-H2 Expression on Gastric Mucosa and Inhibition of Th17 Responses during Helicobacter pylori Infection

Abstract: Gastric epithelial cells (GECs) are the primary target for Helicobacter pylori (H. pylori) infection and may act as antigen presenting cells (APC) regulating local T cell responses. We previously reported that H. pylori infection of GECs induces the expression of the T cell co-inhibitory molecule B7-H1 on GECs. This process contributes to the hyporesponsiveness of CD4+ effector T cells and accumulation of T regulatory cells. In the studies presented herein we investigated the impact of H. pylori cytotoxin CagA… Show more

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Cited by 50 publications
(74 citation statements)
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“…Numerous studies have shown that H. pylori cag pathogenicity island-positive strains are particularly associated with an increased risk of gastric diseases 77 93. Furthermore, it has been recently shown that H. pylori infection downregulates the expression of the T cell co-inhibitory molecule B7-H1 in gastric epithelial cells in a CagA-dependent manner, which might contribute to the hyporesponsiveness of CD4(+) effector T cells and accumulation of Tregs 94. Also, H. pylori infection has been shown to induce the production of the chemokine CCL20 in gastric epithelial cells via cag pathogenicity island-dependent nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling, a phenomenon believed to be involved in Tregs homing to the gastric mucosa as the majority of Tregs express its receptor CCR6 95 .…”
Section: Discussionmentioning
confidence: 99%
“…Numerous studies have shown that H. pylori cag pathogenicity island-positive strains are particularly associated with an increased risk of gastric diseases 77 93. Furthermore, it has been recently shown that H. pylori infection downregulates the expression of the T cell co-inhibitory molecule B7-H1 in gastric epithelial cells in a CagA-dependent manner, which might contribute to the hyporesponsiveness of CD4(+) effector T cells and accumulation of Tregs 94. Also, H. pylori infection has been shown to induce the production of the chemokine CCL20 in gastric epithelial cells via cag pathogenicity island-dependent nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling, a phenomenon believed to be involved in Tregs homing to the gastric mucosa as the majority of Tregs express its receptor CCR6 95 .…”
Section: Discussionmentioning
confidence: 99%
“…1 Chronic gastritis induced by H pylori can progress to atrophic gastritis, intestinal metaplasia, dysplasia, and ultimately gastric cancer (GC). 3 The high levels of the inflammatory reaction to H pylori have been directly linked to the presence of microbial virulence factors, mainly the cagA (cytotoxin-associated gene A) protein. 3 The high levels of the inflammatory reaction to H pylori have been directly linked to the presence of microbial virulence factors, mainly the cagA (cytotoxin-associated gene A) protein.…”
Section: Introductionmentioning
confidence: 99%
“…Because GECs produce IFN-γ (Fig. 3 and (14)) and IFN-γ expression in GECs is completely dependent on IRF8 (Fig. 3), these data suggest that IRF8 could be the major regulator for IFN-γ production in infected gastric tissues.…”
Section: Resultsmentioning
confidence: 84%
“…At 4 and 8 weeks following infection, stomach tissues were processed for histology and tissue culture for enumeration of H. pylori . For infection of cells in vitro , mouse GEC were prepared by enzyme digestion as previously described (14). After culture for 5–8 days, subconfluent cells were incubated with H. pylori with a MOI of 1:100 for 2 days.…”
Section: Methodsmentioning
confidence: 99%