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In this study, we identified USP38, which negatively regulates IL-33-triggered signaling by mediating K27-linked deubiquitination of IL-33R at K511 and its autophagic degradation. USP38 deficiency aggravates IL-33\u2013induced lung inflammatory response and bleomycin-induced pulmonary fibrosis. We further show that the E3 ubiquitin ligase TRAF6 catalyzes K27-linked polyubiquitination of IL-33R at K511, and that deficiency of TRAF6 inhibits IL-33\u2013mediated signaling. Our findings reveal an important mechanism regarding how IL-33R is precisely regulated to ensure its inactivation in rest cells and proper activation following IL-33 stimulation.<\/jats:p>","DOI":"10.1073\/pnas.2116279119","type":"journal-article","created":{"date-parts":[[2022,3,2]],"date-time":"2022-03-02T11:46:46Z","timestamp":1646221606000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":64,"title":["Reciprocal regulation of IL-33 receptor\u2013mediated inflammatory response and pulmonary fibrosis by TRAF6 and USP38"],"prefix":"10.1073","volume":"119","author":[{"given":"Xue-Mei","family":"Yi","sequence":"first","affiliation":[{"name":"Department of Infectious Diseases, Zhongnan Hospital of Wuhan University, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Research Unit of Innate Immune and Inflammatory Diseases, Chinese Academy of Medical Sciences, Wuhan University, Wuhan 430071, 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