{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T00:22:27Z","timestamp":1791418947764,"version":"4.3.3"},"reference-count":133,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2010,10,1]],"date-time":"2010-10-01T00:00:00Z","timestamp":1285891200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2010,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Systemic lupus erythematosus (SLE) is characterized by increased vascular risk due to premature atherosclerosis independent of traditional risk factors. We previously proposed that IFN-\u03b1 plays a crucial role in premature vascular damage in SLE. IFN-\u03b1 alters the balance between endothelial cell apoptosis and vascular repair mediated by endothelial progenitor cells (EPCs) and myeloid circulating angiogenic cells (CACs). In this study, we demonstrate that IFN-\u03b1 promotes an antiangiogenic signature in SLE and control EPCs\/CACs, characterized by transcriptional repression of IL-1\u03b1 and \u03b2, IL-1R1, and vascular endothelial growth factor A, and upregulation of IL-1R antagonist and the decoy receptor IL-1R2. IL-1\u03b2 promotes significant improvement in the functional capacity of lupus EPCs\/CACs, therefore abrogating the deleterious effects of IFN-\u03b1. The beneficial effects from IL-1 are mediated, at least in part, by increases in EPC\/CAC proliferation, by decreases in EPC\/CAC apoptosis, and by preventing the skewing of CACs toward nonangiogenic pathways. IFN-\u03b1 induces STAT2 and 6 phosphorylation in EPCs\/CACs, and JAK inhibition abrogates the transcriptional antiangiogenic changes induced by IFN-\u03b1 in these cells. Immunohistochemistry of renal biopsies from patients with lupus nephritis, but not anti-neutrophil cytoplasmic Ab-positive vasculitis, showed this pathway to be operational in vivo, with increased IL-1R antagonist, downregulation of vascular endothelial growth factor A, and glomerular and blood vessel decreased capillary density, compared with controls. Our study introduces a novel putative pathway by which type I IFNs may interfere with vascular repair in SLE through repression of IL-1\u2013dependent pathways. This could promote atherosclerosis and loss of renal function in this disease.<\/jats:p>","DOI":"10.4049\/jimmunol.1001782","type":"journal-article","created":{"date-parts":[[2010,8,31]],"date-time":"2010-08-31T02:40:37Z","timestamp":1283222437000},"page":"4457-4469","source":"Crossref","is-referenced-by-count":123,"title":["The Detrimental Effects of IFN-\u03b1 on Vasculogenesis in Lupus Are Mediated by Repression of IL-1 Pathways: Potential Role in Atherogenesis and Renal Vascular Rarefaction"],"prefix":"10.1093","volume":"185","author":[{"given":"Seth G","family":"Thacker","sequence":"first","affiliation":[{"name":"Division of Rheumatology, University of Michigan Medical School , Ann Arbor, MI 48109"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Celine C","family":"Berthier","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine, University of Michigan Medical School , Ann Arbor, MI 48109"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deborah","family":"Mattinzoli","sequence":"additional","affiliation":[{"name":"Renal Research Laboratory, Fondazione Istituto di Ricovero e Cura a Carattere Scientifico Ospedale Maggiore Policlinico, Fondazione D'Amico per la Ricerca sulle Malattie Renali , Milan ,","place":["Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria Pia","family":"Rastaldi","sequence":"additional","affiliation":[{"name":"Renal Research Laboratory, Fondazione Istituto di Ricovero e Cura a Carattere Scientifico Ospedale Maggiore Policlinico, Fondazione D'Amico per la Ricerca sulle Malattie Renali , Milan ,","place":["Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthias","family":"Kretzler","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine, University of Michigan Medical School , Ann Arbor, MI 48109"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariana J","family":"Kaplan","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, University of Michigan Medical School , Ann Arbor, MI 48109"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2010,10,1]]},"reference":[{"key":"2025032411582528400_r1","doi-asserted-by":"crossref","first-page":"424","DOI":"10.1016\/S0167-5699(00)01675-3","article-title":"Etiopathogenesis of systemic lupus erythematosus","volume":"21","author":"Herrmann","year":"2000","journal-title":"Immunol. 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