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. 2018 Feb 28;8:3821. doi: 10.1038/s41598-018-20957-2

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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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.