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. 2021 Apr 23;4:499. doi: 10.1038/s42003-021-02018-z

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© The Author(s) 2021

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 — In stage I–II endometriosis, the increased secretion of inflammatory cytokines in ectopic milieu induces FGL2 secretion in Tregs. sFGL2 induces pro-repair macrophages skewing through the suppression of NF-κB and the activation of SHP2-ERK1/2-STAT3 pathway. sFGL2 also up-regulates MT expression in macrophages through STAT3 activation which further promotes pro-repair macrophage polarization. In addition, sFGL2-induced pro-repair macrophages inhibit Th1 and Th17 cell differentiation, while promote Th2 and Tregs differentiation. Taken together, sFGL2 mediated cross-talk between Tregs and macrophage alters the balance of pro- and anti-inflammatory microenvironments and facilitates the formation of immune tolerance in stage III-IV endometriosis.