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. 2021 Feb 5;11:632239. doi: 10.3389/fimmu.2020.632239

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Copyright © 2021 Zhang, Xu, Shao, Sun, Saredy, Cutler, Yao, Liu, Liu, Drummer IV, Lu, Saaoud, Ni, Wang, Li, Li, Jiang, Wang and Yang

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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(A) IPA upstream regulator predictions of upregulated genes in Treg suggest that IL 2 is a universal regulator of Treg in different tissues; and its function could be amplificated from lymphoid tissues to non-lymphoid tissues. We also found that many signature genes we identified were targeted by IL2, such as CTLA4, FOXP3, IKZF2, KLRG1, TNFRSF18, TNFRSF4, etc. (B) IPA Upstream regulator predictions of downregulated genes also suggest that IL 2 is a universal regulator of Treg in non-lymphoid tissues but not in the lymphoid tissues. (C) IPA Upstream regulator predictions of upregulated genes suggesting that NF-kB is a universal regulator of Treg in different tissues except spleen. We found that upregulated signature genes such as FOXP3, IL2RA, TNFRSF4, and IRF4 were parts of NFkB targets, indicating the important role of NFkB in Treg homeostasis.