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. 2021 Apr 13;12:650708. doi: 10.3389/fimmu.2021.650708

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Copyright © 2021 Dang, Lu, Chen and Li

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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Putative mechanism underlying the effect of baricitinib on experimental autoimmune encephalomyelitis (EAE). Phosphorylation of receptor chains by JAKs is induced by cytokine binding. STAT1, STAT3, and STAT4 are phosphorylated by JAK1 and JAK2, leading to dimerization. Baricitinib inhibited JAK1 and JAK2, leading to decreased phosphorylation of STAT1, STAT3, and STAT4. The reduction in STAT3 phosphorylation may directly inhibit Th 17 cell differentiation. The reduction in STAT1 and STAT4 phosphorylation suppresses Th 1 cell differentiation. SEM, standard error of the mean.