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. 2022 Jan 12;7:3. doi: 10.1038/s41536-021-00196-2

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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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Fig. 10 — Shh, secreted from the gastric parietal cells in response to acute injury to the stomach induced macrophage chemotaxis and subsequently CD44v9-expressing SPEM. Shh acts as a macrophage chemoattractant via a smoothened-dependent mechanism. IL-33 is released from the injured epithelium, and macrophages drive the polarization of macrophages to an M2 phenotype. IL-13, released from recruited ILC2 cells, subsequently regulates the development of CD44v9-expressing SPEM, which is crucial for the regeneration of the gastric epithelium.