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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 \u03b1-glucoside (\u03b1CAG) and cholesteryl phosphatidyl \u03b1-glucoside (\u03b1CPG) were identified as noncanonical ligands for Mincle (Clec4e) and DCAR (Clec4b1). During chronic infection, H. pylori\u2013specific T cell responses and gastritis were ameliorated in Mincle-deficient mice, although bacterial burdens remained unchanged. Furthermore, a mutant H. pylori strain lacking \u03b1CAG and \u03b1CPG exhibited an impaired ability to cause gastritis. Thus H. pylori\u2013specific modification of host cholesterol plays a pathophysiological role that exacerbates gastric inflammation by triggering C-type lectin receptors.<\/jats:p>","DOI":"10.1084\/jem.20200815","type":"journal-article","created":{"date-parts":[[2020,8,19]],"date-time":"2020-08-19T02:22:07Z","timestamp":1597803727000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":73,"title":["<i>Helicobacter pylori<\/i>\n                    metabolites exacerbate gastritis through C-type lectin receptors"],"prefix":"10.1084","volume":"218","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2748-619X","authenticated-orcid":true,"given":"Masahiro","family":"Nagata","sequence":"first","affiliation":[{"name":"Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan 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