Figure 7
A schematic diagram illustrates a novel regulatory pathway controlling gastric mucosal immunity, wherein a C-type lectin receptor (CLR), COLEC12, is important in bridging H. pylori-mediated crosstalk between gastric stromal cells (GSCs) and DCs within the gastric mucosa. Hp can disrupt the epithelial barrier and transit to the sub-epithelial mucosal layer, where the contact between Hp and GSCs is possible and critical in controlling Hp-mediated inflammation. Subsequent to the Hp-stromal cell interaction, PGE2-dependent conditioning effect on DCs is noted and PGE2 released from Hp treated GSCs is negatively regulated by GM-CSF and shown to be able to induce IL-23 secretion in DCs.
