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. 2021 Aug 26;12:741839. doi: 10.3389/fimmu.2021.741839

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Copyright © 2021 Tang, Li, Zhou, Wang, Fan, Yang and Qi

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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Model of the function and mechanism of TRIM65-mediated inhibition of NLRP3 inflammasome activation. TRIM65 directly binds NLRP3 and promotes K48- and K63- linked ubiquitination, which is critical for the inhibition of NLRP3 inflammasome activation in resting and priming macrophages. With stimulation of priming signals (for example LPS-TLR4-Myd88-NF-κB) and PAMPs or DAMPs (such as MSU, ATP, R837, Nigericin, etc.), TRIM65 significantly decreased, follow by attenuated ubiquitination of NLRP3, strengthened NLRP3-NEK7 interaction, assembled and activated NLRP3 inflammasome. (PAMPs, pathogen-associated molecular patterns; DAMPs, danger-associated molecular patterns).