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. 2020 Jan 17;10:3003. doi: 10.3389/fimmu.2019.03003

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Copyright © 2020 Ji, Liao, Rao, Li, Yang, Yuan, Feng, Xu, Shao and Su.

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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Schematic comparison between CiTLR22a- and CiTLR22b-mediated signaling pathways. Both CiTLR22a and CiTLR22b localize to lysosome, recognize dsRNA, and recruit MyD88 adaptor molecule. CiTLR22a inhibits IRAK3 expression, enhances the protein and phosphorylation levels of IRF7, and facilitates the IFN and NF-κB pathways. However, CiTLR22b promotes IRAK3 expression, inhibits the phosphorylation level of IRF7 and protein level of IRF3, and plays a negative role in initiating the IFN and NF-κB pathways.