RT Journal Article SR Electronic T1 A pro-inflammatory role for Th22 cells in Helicobacter pylori-associated gastritis JF Gut JO Gut FD BMJ Publishing Group Ltd and British Society of Gastroenterology SP 1368 OP 1378 DO 10.1136/gutjnl-2014-307020 VO 64 IS 9 A1 Zhuang, Yuan A1 Cheng, Ping A1 Liu, Xiao-fei A1 Peng, Liu-sheng A1 Li, Bo-sheng A1 Wang, Ting-ting A1 Chen, Na A1 Li, Wen-hua A1 Shi, Yun A1 Chen, Weisan A1 Pang, Ken C A1 Zeng, Ming A1 Mao, Xu-hu A1 Yang, Shi-ming A1 Guo, Hong A1 Guo, Gang A1 Liu, Tao A1 Zuo, Qian-fei A1 Yang, Hui-jie A1 Yang, Liu-yang A1 Mao, Fang-yuan A1 Lv, Yi-pin A1 Zou, Quan-ming YR 2015 UL http://gut.bmj.com/content/64/9/1368.abstract AB Objective Helper T (Th) cell responses are critical for the pathogenesis of Helicobacter pylori-induced gastritis. Th22 cells represent a newly discovered Th cell subset, but their relevance to H. pylori-induced gastritis is unknown.Design Flow cytometry, real-time PCR and ELISA analyses were performed to examine cell, protein and transcript levels in gastric samples from patients and mice infected with H. pylori. Gastric tissues from interleukin (IL)-22-deficient and wild-type (control) mice were also examined. Tissue inflammation was determined for pro-inflammatory cell infiltration and pro-inflammatory protein production. Gastric epithelial cells and myeloid-derived suppressor cells (MDSC) were isolated, stimulated and/or cultured for Th22 cell function assays.Results Th22 cells accumulated in gastric mucosa of both patients and mice infected with H. pylori. Th22 cell polarisation was promoted via the production of IL-23 by dendritic cells (DC) during H. pylori infection, and resulted in increased inflammation within the gastric mucosa. This inflammation was characterised by the CXCR2-dependent influx of MDSCs, whose migration was induced via the IL-22-dependent production of CXCL2 by gastric epithelial cells. Under the influence of IL-22, MDSCs, in turn, produced pro-inflammatory proteins, such as S100A8 and S100A9, and suppressed Th1 cell responses, thereby contributing to the development of H. pylori-associated gastritis.Conclusions This study, therefore, identifies a novel regulatory network involving H. pylori, DCs, Th22 cells, gastric epithelial cells and MDSCs, which collectively exert a pro-inflammatory effect within the gastric microenvironment. Efforts to inhibit this Th22-dependent pathway may therefore prove a valuable strategy in the therapy of H. pylori-associated gastritis.