{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T07:06:20Z","timestamp":1791270380338,"version":"4.1.0"},"reference-count":56,"publisher":"Rockefeller University Press","issue":"10","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,9,22]]},"abstract":"<jats:p>Plasmacytoid dendritic cells (pDCs) have long been implicated in the pathogenesis of lupus. However, this conclusion has been largely based on a correlative link between the copious production of IFN-\u03b1\/\u03b2 by pDCs and the IFN-\u03b1\/\u03b2 \u201csignature\u201d often seen in human lupus patients. The specific contribution of pDCs to disease in vivo has not been investigated in detail. For this reason, we generated a strain of BXSB lupus-prone mice in which pDCs can be selectively depleted in vivo. Early, transient ablation of pDCs before disease initiation resulted in reduced splenomegaly and lymphadenopathy, impaired expansion and activation of T and B cells, reduced antibodies against nuclear autoantigens and improved kidney pathology. Amelioration of pathology coincided with decreased transcription of IFN-\u03b1\/\u03b2\u2013induced genes in tissues. PDC depletion had an immediate impact on the activation of immune cells, and importantly, the beneficial effects on pathology were sustained even though pDCs later recovered, indicating an early pDC contribution to disease. Together, our findings demonstrate a critical function for pDCs during the IFN-\u03b1\/\u03b2\u2013dependent initiation of autoimmune lupus and point to pDCs as an attractive therapeutic target for the treatment of SLE.<\/jats:p>","DOI":"10.1084\/jem.20132620","type":"journal-article","created":{"date-parts":[[2014,9,2]],"date-time":"2014-09-02T00:19:08Z","timestamp":1409617148000},"page":"1977-1991","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":269,"title":["Early, transient depletion of plasmacytoid dendritic cells ameliorates autoimmunity in a lupus model"],"prefix":"10.1084","volume":"211","author":[{"given":"Sarah L.","family":"Rowland","sequence":"first","affiliation":[{"name":"Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey M.","family":"Riggs","sequence":"additional","affiliation":[{"name":"Respiratory, Inflammation and Autoimmunity Research Department, MedImmune, Gaithersburg, MD 20878 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susan","family":"Gilfillan","sequence":"additional","affiliation":[{"name":"Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mattia","family":"Bugatti","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Brescia, 25123 Brescia, Italy 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William","family":"Vermi","sequence":"additional","affiliation":[{"name":"Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110 1"},{"name":"Department of Pathology, University of Brescia, 25123 Brescia, Italy 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roland","family":"Kolbeck","sequence":"additional","affiliation":[{"name":"Respiratory, Inflammation and Autoimmunity Research Department, MedImmune, Gaithersburg, MD 20878 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emil R.","family":"Unanue","sequence":"additional","affiliation":[{"name":"Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miguel A.","family":"Sanjuan","sequence":"additional","affiliation":[{"name":"Respiratory, Inflammation and Autoimmunity Research Department, MedImmune, Gaithersburg, MD 20878 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marco","family":"Colonna","sequence":"additional","affiliation":[{"name":"Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110 1"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2014,9,1]]},"reference":[{"key":"2023072602043811200_bib1","doi-asserted-by":"publisher","first-page":"305","DOI":"10.1182\/blood-2002-04-1088","article-title":"Essential role for ICSBP in the in vivo development of murine CD8alpha + dendritic cells","volume":"101","author":"Aliberti","year":"2003","journal-title":"Blood."},{"key":"2023072602043811200_bib2","doi-asserted-by":"publisher","first-page":"2293","DOI":"10.4049\/jimmunol.170.5.2293","article-title":"The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells","volume":"170","author":"Amano","year":"2003","journal-title":"J. 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