A proposed model of cross-talk among Helicobacter pylori, dendritic cells (DC), gastric epithelial cells and myeloid-derived suppressor cells (MDSC) leading.

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Presentation transcript:

A proposed model of cross-talk among Helicobacter pylori, dendritic cells (DC), gastric epithelial cells and myeloid-derived suppressor cells (MDSC) leading to Th22 cell differentiation and MDSC-mediated proinflammation in gastric mucosa during H. pylori infection. A proposed model of cross-talk among Helicobacter pylori, dendritic cells (DC), gastric epithelial cells and myeloid-derived suppressor cells (MDSC) leading to Th22 cell differentiation and MDSC-mediated proinflammation in gastric mucosa during H. pylori infection. H. pylori stimulate DCs to secrete interleukin (IL)-23 and H. pylori induce gastric epithelial cells to express IL-22R1. Release of IL-23 induces the polarisation of Th22 cells. Polarised Th22 cells expand in gastric mucosa where they release cytokine IL-22 that stimulates gastric epithelial cells to secrete CXCL2. Responding to the CXCL2 chemokine gradient, myeloid progenitor cell-derived, CXCR2-expressing MDSCs migrate into gastric mucosa where they exert a proinflammatory effect by producing inflammatory proteins, S100A8 and S100A9, and suppressing T helper type 1 (Th1) cell response. Yuan Zhuang et al. Gut 2015;64:1368-1378 Copyright © BMJ Publishing Group Ltd & British Society of Gastroenterology. All rights reserved.