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. 2021 May 7;12:680068. doi: 10.3389/fimmu.2021.680068

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Copyright © 2021 Zhang, Yang, Jing, Zhai, Zhang, Ma, Li, Yan, Cheng, Zhang, Ning, Shi, Wang, Zhao, Dai, Li, Ming, Yu, Wang, Cheng, Xiong and Dong

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 model of the mechanism whereby PKM2 participates in the pathogenesis of TLRs-mediated inflammation and autoimmunity. This schematic shows that hyper-activation of TLRs lead to PKM2 over-expression and PKM2 augments TLR4/TLR7/TLR9-induced activations of macrophages, DCs and B cells by promoting Pyk2 activation, thereby contributing to the pathogenesis of TLRs-mediated inflammation and autoimmunity. Pharmaceutical inhibition of PKM2 by PKM2-IN can inhibit TLR4/TLR7/TLR9-induced activations of macrophages, DCs and B cells, and alleviate the pathogenesis of TLRs-mediated inflammation and autoimmunity.