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- W4313348199 abstract "Abstract CD4+ T cells are recruited to the gastric mucosa during H. pylori infection, but are generally hyporesponsive. CD4+CD25+FoxP3+ regulatory T cells (Treg) are present during infection and impact the CD4+ T cell response. We have previously shown that epithelial cell responses to H. pylori play an important role in inhibiting CD4+ T cell responses via the local induction of Treg cells from naïve CD4+ T cells. As TGF-β plays a role in the development of Tregs, we hypothesized that gastric epithelial cells (GECs) produce TGF-β during H. pylori infection that contributes to Treg development and suppresses local CD4+ T cell effector function. In order to investigate this, we examined GEC production of TGF-β after exposure to H. pylori and found them to produce significant levels of TGF-β that were partially dependant on the cag PAI virulence factor of H. pylori. TGF-β produced by GEC in response to H. pylori increased the local development of CD4+CD25+FoxP3+ Treg cells from naïve T cells in co-culture with GEC and decreased proliferation of activated CD4+ T effector cells in co-culture with GEC. These events were decreased when TGF-β neutralizing antibodies were present. The observations presented here introduce a novel mechanism used by H. pylori via gastric epithelial cells leading to inhibition of CD4+ T cells that may contribute to chronicity of infection." @default.
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- W4313348199 date "2009-04-01" @default.
- W4313348199 modified "2023-09-29" @default.
- W4313348199 title "<i>Helicobacter pylori</i> Induces Gastric Epithelial Cell Production of TGF-β that Suppresses CD4+ T Cells (97.7)" @default.
- W4313348199 doi "https://doi.org/10.4049/jimmunol.182.supp.97.7" @default.
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