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. 2022 Mar 5;22:108. doi: 10.1186/s12935-022-02528-8

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Plasticity of Th17. Th17 cells can mainly transform into TFH, Th2, TR1, Treg, and Th1 cells and exhibit a variety of contrasting functions depending on environmental conditions. During infections and autoimmune diseases, Th17 cells can acquire immune inhibitory functions by becoming TR1 or Treg cells. Th17 cells also change to TFH cells at a steady-state and participate in promoting IgA-producing B cells. Also, Th17 cells acquire pathogenic activity by changing to Th2 cells during asthma or Th1 cells during infection, cancer, and autoimmune diseases