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Although <jats:italic>H. pylori<\/jats:italic>\u2010induced inflammation is a key inducer of precancerous lesions in the gastric mucosa, it remains unclear which precise immune cell subsets are responsible for the progression of <jats:italic>H. pylori<\/jats:italic>\u2010induced gastritis. Here, we observed an abundance of CD4<jats:sup>+<\/jats:sup>IL\u201017A<jats:sup>+<\/jats:sup>FOXP3<jats:sup>+<\/jats:sup> T cells exhibiting a Th17\u2010like phenotype within the microenvironment of <jats:italic>H. pylori<\/jats:italic>\u2010induced gastritis. Mechanistically, <jats:italic>H. pylori<\/jats:italic> upregulated the expression of IL\u20106 in Dendritic cells and macrophages, by activating NF\u2010\u03baB signaling through the virulence factor CagA and thus, induced IL\u201017A expression in FOXP3<jats:sup>+<\/jats:sup> T cells. Moreover, CD4<jats:sup>+<\/jats:sup>IL\u201017A<jats:sup>+<\/jats:sup>FOXP3<jats:sup>+<\/jats:sup> T cells were positively associated with advanced precancerous lesions. Therefore, these findings offer essential insights into how FOXP3<jats:sup>+<\/jats:sup> T cells sense inflammatory signals from the environment, such as IL\u20106, during <jats:italic>H.\u2009pylori<\/jats:italic> infections, thereby guiding the effector immune response and aggravating the gastritis.<\/jats:p>","DOI":"10.1002\/eji.202350662","type":"journal-article","created":{"date-parts":[[2024,2,17]],"date-time":"2024-02-17T11:40:11Z","timestamp":1708170011000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Increased infiltration of CD4<sup>+<\/sup>IL\u201017A<sup>+<\/sup>FOXP3<sup>+<\/sup> T cells in <i>Helicobacter\u2009pylori<\/i>\u2010induced gastritis"],"prefix":"10.1002","volume":"54","author":[{"given":"Yixian","family":"Guo","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology Shanghai Institute of Digestive Disease \u00a0NHC Key Laboratory of Digestive Diseases 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