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. 2021 Jan 12;12(1):79. doi: 10.1038/s41419-021-03395-3

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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. 3 — TGF-β stimulates Smad2 and Smad3, thereby activating Foxp3 and promoting Treg cell differentiation. TGF-β and IL-6 together stimulate JAK kinases and transcription factors STAT3 and STAT5, subsequently activating RORγt and Th17 cell generation. MST1/2 enhances the stability of Foxp3 and promotes Treg cell generation through LATS1/2, NDR1/2, and YAP. In contrast, TAZ inhibits foxp3 and attenuates Treg cell generation but promotes the process of Th17 cell generation. In addition, TEAD1 may hinder Th17 cell formation. Arrows and blunt ends indicate activation and repression, respectively.