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. 2019 Oct 31;10:2532. doi: 10.3389/fimmu.2019.02532

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Copyright © 2019 Yuan, Xu, Liu, Liu, Huang 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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Interleukin (IL)-36 signal pathways induce inflammatory responses. Pro-IL-36 cytokines are inactive proteins and require post-translational processing to fully unleash the pro-inflammatory activity. IL-36 agonists bind to heterodimeric receptor complexes, including IL-36 receptor (IL-36R) and co-receptor IL-1 receptor accessory protein (IL-1RAcP). Subsequently, the heterotrimer complex binds to adaptor protein myeloid differentiated protein 88 (MyD88), activating mitogen-activated protein kinase (MAPK) and nuclear transcription factor kappa B (NF-κB) signaling cascade pathways, and regulates expression of target genes.