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• W2559981308 abstract "Abstract Background We previously demonstrated that H. pylori infection leads to increased induction of regulatory T cells in local and systemic immune compartments. Here, we investigate the role of CCR 2 in the tolerogenic programing of dendritic cells in a mouse model of H. pylori infection. Materials and Methods CCR 2 deficient ( CCR 2 KO ) mice and wild‐type (Wt) mice infected with H. pylori SS 1 strain were analyzed by qPCR and FACS analysis. In vitro, bone marrow‐derived DC on day 6 from CCR 2 KO and Wt mice cocultured with or without H. pylori were examined to determine the impact of CCR 2 signaling on dendritic cells function by qPCR , ELISA , and FACS analyses. Results Acute H. pylori infection was associated with a threefold increase in CCR 2 mRNA expression in the gastric mucosa. H. pylori ‐infected CCR 2 KO mice exhibited a higher degree of mucosal inflammation, that is, increased gastritis scores and pro‐inflammatory cytokine mRNA levels, but lower degree of H. pylori gastric colonization compared to infected Wt mice. Peripheral H. pylori ‐specific immune response measured in the CCR 2 KO spleen was characterized by a higher Th17 response and a lower Treg response. In vitro, CCR 2 KO bone marrow‐derived DC was less mature and shown a lower Treg/Th17 ratio. Moreover, blockade of CCR 2 signaling by MCP ‐1 neutralizing antibody inhibited H. pylori ‐stimulated bone marrow‐derived DC maturation. Conclusions Our results indicate that CCR 2 plays an essential role in H. pylori ‐induced immune tolerance and shed light on a novel mechanism of CCR 2‐dependent DC Treg induction, which appears to be important in maintaining mucosal homeostasis during H. pylori infection." @default.
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• W2559981308 date "2016-12-08" @default.
• W2559981308 modified "2023-09-27" @default.
• W2559981308 title "CCR2 mediates<i>Helicobacter pylori</i>-induced immune tolerance and contributes to mucosal homeostasis" @default.
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• W2559981308 doi "https://doi.org/10.1111/hel.12366" @default.
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