{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,19]],"date-time":"2026-06-19T21:56:25Z","timestamp":1781906185422,"version":"3.54.5"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2025,3,6]],"date-time":"2025-03-06T00:00:00Z","timestamp":1741219200000},"content-version":"vor","delay-in-days":3017,"URL":"https:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Polymorphisms in the TNIP1 gene encoding A20-binding inhibitor of NF-\u03baB1 (ABIN1) predispose to lupus and other autoimmune diseases in at least eight human populations. We found previously that knock-in mice expressing a ubiquitin-binding\u2013defective mutant of ABIN1 (ABIN1[D485N]) develop autoimmunity as they age and succumb to a disease resembling lupus nephritis in humans. In this article, we report that Flt3-derived dendritic cells from these mice overproduced type 1 IFNs upon stimulation with ligands that activate TLR7 or TLR9. However, crossing ABIN1[D485N] mice to IFNAR1-knockout mice that do not express the \u03b1-subunit of the type 1 IFNR did not prevent splenomegaly, the appearance of high serum levels of autoantibodies and other Igs, or liver inflammation and only reduced kidney inflammation modestly. In contrast, crossing ABIN1[D485N] mice to knock-in mice expressing catalytically inactive mutants of IRAK1 or IRAK4 prevented splenomegaly, autoimmunity, and liver and kidney inflammation. Our results support the notion that IRAK1 and\/or IRAK4 are attractive targets for the development of drugs to prevent, and perhaps treat, lupus nephritis and other autoinflammatory diseases caused by the decreased ability of ABIN1 or other proteins to restrict the strength of MyD88 signaling.<\/jats:p>","DOI":"10.4049\/jimmunol.1600788","type":"journal-article","created":{"date-parts":[[2016,11,3]],"date-time":"2016-11-03T02:03:34Z","timestamp":1478138614000},"page":"4266-4273","source":"Crossref","is-referenced-by-count":51,"title":["Suppression of IRAK1 or IRAK4 Catalytic Activity, but Not Type 1 IFN Signaling, Prevents Lupus Nephritis in Mice Expressing a Ubiquitin Binding\u2013Defective Mutant of ABIN1"],"prefix":"10.1093","volume":"197","author":[{"given":"Sambit K","family":"Nanda","sequence":"first","affiliation":[{"name":"Medical Research Council Protein Phosphorylation and Ubiquitylation Unit, University of Dundee , Dundee DD1 5EH,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marta","family":"Lopez-Pelaez","sequence":"additional","affiliation":[{"name":"Medical Research Council Protein Phosphorylation and Ubiquitylation Unit, University of Dundee , Dundee DD1 5EH,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J Simon C","family":"Arthur","sequence":"additional","affiliation":[{"name":"Division of Immunology and Cell Signaling, School of Life Sciences, University of Dundee , Dundee DD1 5EH,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1179-5788","authenticated-orcid":false,"given":"Francesco","family":"Marchesi","sequence":"additional","affiliation":[{"name":"School of Veterinary Medicine, University of Glasgow , Glasgow G61 1QH,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philip","family":"Cohen","sequence":"additional","affiliation":[{"name":"Medical Research Council Protein Phosphorylation and Ubiquitylation Unit, University of Dundee , Dundee DD1 5EH,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2016,12,1]]},"reference":[{"key":"2025030618355969800_r1","doi-asserted-by":"crossref","first-page":"1215","DOI":"10.1084\/jem.20102177","article-title":"Polyubiquitin binding to ABIN1 is required to prevent autoimmunity","volume":"208","author":"Nanda","year":"2011","journal-title":"J. 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