{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T17:56:41Z","timestamp":1780077401747,"version":"3.54.0"},"reference-count":81,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2024,4,12]],"date-time":"2024-04-12T00:00:00Z","timestamp":1712880000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R56AI148785"],"award-info":[{"award-number":["R56AI148785"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["4T32AI106677-05"],"award-info":[{"award-number":["4T32AI106677-05"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,6,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Plasmacytoid dendritic cells (pDCs) are strongly implicated as a major source of IFN-I in systemic lupus erythematosus (SLE), triggered through TLR-mediated recognition of nucleic acids released from dying cells. However, relatively little is known about how TLR signaling and IFN-I production are regulated in pDCs. In this article, we describe a role for integrin \u03b1v\u03b23 in regulating TLR responses and IFN-I production by pDCs in mouse models. We show that \u03b1v and \u03b23-knockout pDCs produce more IFN-I and inflammatory cytokines than controls when stimulated through TLR7 and TLR9 in vitro and in vivo. Increased cytokine production was associated with delayed acidification of endosomes containing TLR ligands, reduced LC3 conjugation, and increased TLR signaling. This dysregulated TLR signaling results in activation of B cells and promotes germinal center (GC) B cell and plasma cell expansion. Furthermore, in a mouse model of TLR7-driven lupus-like disease, deletion of \u03b1v\u03b23 from pDCs causes accelerated autoantibody production and pathology. We therefore identify a pDC-intrinsic role for \u03b1v\u03b23 in regulating TLR signaling and preventing activation of autoreactive B cells. Because \u03b1v\u03b23 serves as a receptor for apoptotic cells and cell debris, we hypothesize that this regulatory mechanism provides important contextual cues to pDCs and functions to limit responses to self-derived nucleic acids.<\/jats:p>","DOI":"10.4049\/jimmunol.2300290","type":"journal-article","created":{"date-parts":[[2024,4,12]],"date-time":"2024-04-12T13:48:33Z","timestamp":1712929713000},"page":"1680-1692","source":"Crossref","is-referenced-by-count":6,"title":["Integrin \u03b1v\u03b23 Limits Cytokine Production by Plasmacytoid Dendritic Cells and Restricts TLR-Driven Autoimmunity"],"prefix":"10.1093","volume":"212","author":[{"given":"Alina K","family":"Lorant","sequence":"first","affiliation":[{"name":"Benaroya Research Institute at Virginia Mason , Seattle, WA"},{"name":"Department of Immunology, University of Washington , Seattle, WA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-3717-1992","authenticated-orcid":false,"given":"Anna E","family":"Yoshida","sequence":"additional","affiliation":[{"name":"Benaroya Research Institute at Virginia Mason , Seattle, WA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emily A","family":"Gilbertson","sequence":"additional","affiliation":[{"name":"Benaroya Research Institute at Virginia Mason , Seattle, WA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Talyn","family":"Chu","sequence":"additional","affiliation":[{"name":"Benaroya Research Institute at Virginia Mason , Seattle, WA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3420-432X","authenticated-orcid":false,"given":"Caroline","family":"Stefani","sequence":"additional","affiliation":[{"name":"Benaroya Research Institute at Virginia Mason , Seattle, WA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mridu","family":"Acharya","sequence":"additional","affiliation":[{"name":"Seattle Children\u2019s Research Institute , Seattle, WA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5864-5299","authenticated-orcid":false,"given":"Jessica A","family":"Hamerman","sequence":"additional","affiliation":[{"name":"Benaroya Research Institute at Virginia Mason , Seattle, WA"},{"name":"Department of Immunology, University of Washington , Seattle, WA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2162-0156","authenticated-orcid":false,"given":"Adam","family":"Lacy-Hulbert","sequence":"additional","affiliation":[{"name":"Benaroya Research Institute at Virginia Mason , Seattle, WA"},{"name":"Department of Immunology, University of Washington , Seattle, WA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2024,4,12]]},"reference":[{"key":"2025020405500140800_r1","doi-asserted-by":"crossref","first-page":"1491","DOI":"10.1002\/art.21031","article-title":"Activation of the interferon-alpha pathway identifies a subgroup of systemic lupus erythematosus patients with distinct serologic features and active disease","volume":"52","author":"Kirou","year":"2005","journal-title":"Arthritis Rheum."},{"key":"2025020405500140800_r2","doi-asserted-by":"crossref","first-page":"2610","DOI":"10.1073\/pnas.0337679100","article-title":"Interferon-inducible gene expression signature in peripheral blood cells of patients with severe lupus","volume":"100","author":"Baechler","year":"2003","journal-title":"Proc. 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