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We found that the STING S365A mutation, which abrogates IRF3 binding and type I interferon induction, rescued the embryonic lethality of DNase II\u2212\/\u2212 mice. However, the STING S365A mutant retains the ability to recruit TBK1 and activate NF-\u03baB, and DNase II\u2212\/\u2212STING-S365A mice exhibited severe polyarthritis, which was alleviated by neutralizing antibodies against TNF-\u03b1 or IL-6 receptor. In contrast, the STING L373A mutation or C-terminal tail truncation, which disrupts TBK1 binding and therefore prevents activation of both IRF3 and NF-\u03baB, completely rescued the phenotypes of DNase II\u2212\/\u2212 mice. These results demonstrate that TBK1 recruitment to STING mediates autoinflammatory arthritis independently of type I interferons. Inhibiting TBK1 binding to STING may be a therapeutic strategy for certain autoinflammatory diseases instigated by self-DNA.<\/jats:p>","DOI":"10.1084\/jem.20211539","type":"journal-article","created":{"date-parts":[[2021,11,18]],"date-time":"2021-11-18T02:22:07Z","timestamp":1637202127000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":49,"title":["TBK1 recruitment to STING mediates autoinflammatory arthritis caused by defective DNA clearance"],"prefix":"10.1084","volume":"219","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3725-1420","authenticated-orcid":true,"given":"Tong","family":"Li","sequence":"first","affiliation":[{"name":"Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 1"},{"name":"Center for Inflammation Research, University of Texas Southwestern Medical Center, Dallas, TX 2"},{"name":"Department of Rheumatology and Immunology, Xiangya Hospital, Central South University, Changsha, Hunan, China 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0226-4774","authenticated-orcid":true,"given":"Seoyun","family":"Yum","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 1"},{"name":"Center for Inflammation Research, University of Texas Southwestern Medical Center, Dallas, TX 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1456-2691","authenticated-orcid":true,"given":"Minghao","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 1"},{"name":"Center for Inflammation Research, University of Texas Southwestern Medical Center, Dallas, TX 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6608-3211","authenticated-orcid":true,"given":"Xiang","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 1"},{"name":"Center for Inflammation Research, University of Texas Southwestern Medical Center, Dallas, TX 2"},{"name":"Howard Hughes Medical Institute, Chevy Chase, MD 4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3928-9660","authenticated-orcid":true,"given":"Xiaoxia","family":"Zuo","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Immunology, Xiangya Hospital, Central South University, Changsha, Hunan, China 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8475-8251","authenticated-orcid":true,"given":"Zhijian J.","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 1"},{"name":"Center for Inflammation Research, University of Texas Southwestern Medical Center, Dallas, TX 2"},{"name":"Howard Hughes Medical Institute, Chevy Chase, MD 4"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2021,12,13]]},"reference":[{"key":"2023072812492656200_bib1","doi-asserted-by":"publisher","first-page":"5328","DOI":"10.1128\/JVI.00037-14","article-title":"Cytosolic-DNA-mediated, STING-dependent proinflammatory gene induction necessitates canonical NF-\u03baB activation through TBK1","volume":"88","author":"Abe","year":"2014","journal-title":"J. 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