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. 2021 May 13;12:662266. doi: 10.3389/fimmu.2021.662266

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Copyright © 2021 Wang, Yi and Liang

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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In COVID-19 patients, SARS-CoV-2 may promote hyperinflammation in the lung and exacerbate tissue damage. IL-36-activated inflammatory immune cells (e.g., monocytes, macrophages, neutrophils and pathogenic T cells) produce IL-6, IL-1, IL-17, TNF-α and GM-CSF to further amplify IL-36 responses. IL-36Ra and IL-38, as the natural antagonistic mediators in IL-36 family might be a promising therapeutic target for COVID-19 via inhibiting IL-36 signaling pathway and alleviating pulmonary hyperinflammation.