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. 2017 Aug 10;7:7812. doi: 10.1038/s41598-017-07573-2

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© The Author(s) 2017

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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Postulated model showing the cardioprotective effects of TDAG8-expressing cardiac macrophages against MI. MI induces a pH reduction and severe inflammation at infarcted areas. TDAG8 expressed on cardiac macrophages recognises extracellular pH changes and inhibits the Ccl20 transcription stimulated by inflammatory factors (e.g. HMGB1 and TNF-α), which inhibits the recruitment of IL-17A-producing CCR6⁺ γδT cells. These cells are mediators of cell death and fibrosis, thus explaining the cardioprotective effects of TDAG8.