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- W3090446835 abstract "Helicobacter pylori causes gastritis, which has been attributed to the development of H. pylori–specific T cells during infection. However, the mechanism underlying innate immune detection leading to the priming of T cells is not fully understood, as H. pylori evades TLR detection. Here, we report that H. pylori metabolites modified from host cholesterol exacerbate gastritis through the interaction with C-type lectin receptors. Cholesteryl acyl α-glucoside (αCAG) and cholesteryl phosphatidyl α-glucoside (αCPG) were identified as noncanonical ligands for Mincle (Clec4e) and DCAR (Clec4b1). During chronic infection, H. pylori–specific T cell responses and gastritis were ameliorated in Mincle-deficient mice, although bacterial burdens remained unchanged. Furthermore, a mutant H. pylori strain lacking αCAG and αCPG exhibited an impaired ability to cause gastritis. Thus H. pylori–specific modification of host cholesterol plays a pathophysiological role that exacerbates gastric inflammation by triggering C-type lectin receptors." @default.
- W3090446835 created "2020-10-08" @default.
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- W3090446835 date "2020-09-29" @default.
- W3090446835 modified "2023-10-18" @default.
- W3090446835 title "Helicobacter pylori metabolites exacerbate gastritis through C-type lectin receptors" @default.
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- W3090446835 doi "https://doi.org/10.1084/jem.20200815" @default.
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- W3090446835 hasPublicationYear "2020" @default.
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