{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T22:34:40Z","timestamp":1781303680196,"version":"3.54.1"},"reference-count":18,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2015,7,28]],"date-time":"2015-07-28T00:00:00Z","timestamp":1438041600000},"content-version":"vor","delay-in-days":88,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"NIH (National Institute of Arthritis and Musculoskeletal and Skin Diseases Intramural Research Program)"},{"name":"Heart and Stroke Foundation of Canada"},{"name":"NIH","award":["T32-HD-7513-15"],"award-info":[{"award-number":["T32-HD-7513-15"]}]},{"name":"US Public Health Service"},{"name":"Charles Woodson Biostatistics Award"},{"name":"North West England Medical Research Council Clinical Pharmacology and Therapeutics Training Scheme","award":["G1000417\/94909"],"award-info":[{"award-number":["G1000417\/94909"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatology"],"published-print":{"date-parts":[[2015,5]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>Systemic lupus erythematosus (SLE) is characterized by increased cardiovascular risk in adult\u2010onset and childhood\u2010onset SLE. Type I interferons (IFNs) appear to play a prominent role in premature vascular damage in adult\u2010onset SLE, at least in part, by inducing impairments in the phenotype and function of endothelial progenitor cells (EPCs), thereby hampering vascular repair. It is not clear whether EPC dysfunction is present in childhood\u2010onset SLE in association with a type I IFN signature.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The phenotype and numbers of EPCs were quantified in patients with childhood\u2010onset SLE, patients with juvenile idiopathic arthritis (JIA), and matched healthy control subjects. In a separate cohort of patients with childhood\u2010onset SLE, markers of subclinical atherosclerosis and endothelial dysfunction were quantified using standardized protocols and analyzed for associations with serum type I IFN activity.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>EPC numbers and function were significantly decreased in patients with childhood\u2010onset SLE compared with patients with JIA and healthy control subjects. Serum from patients with childhood\u2010onset SLE impaired differentiation of EPCs into mature endothelial cells in healthy controls, and this effect was blocked by inhibition of the type I IFN pathway. Type I IFN activity in serum was not significantly associated with subclinical atherosclerosis and endothelial function in patients with childhood\u2010onset SLE.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>As in adult\u2010onset SLE, childhood\u2010onset SLE is characterized by phenotypic and functional EPC abnormalities, which are likely triggered by type I IFNs. Although cross\u2010sectional analysis revealed no global association between type I IFN signatures and vascular measures of subclinical atherosclerosis, longitudinal assessments are needed to evaluate whether progression of vascular damage in patients with childhood\u2010onset SLE is associated with type I IFNs, as observed in patients with adult\u2010onset SLE.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.39149","type":"journal-article","created":{"date-parts":[[2015,4,17]],"date-time":"2015-04-17T11:02:11Z","timestamp":1429268531000},"page":"2257-2262","source":"Crossref","is-referenced-by-count":35,"title":["Brief Report: Endothelial Progenitor Cell Phenotype and Function Are Impaired in Childhood\u2010Onset Systemic Lupus Erythematosus"],"prefix":"10.1002","volume":"67","author":[{"given":"Smriti","family":"Mohan","sequence":"first","affiliation":[{"name":"University of Michigan Ann Arbor"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie","family":"Barsalou","sequence":"additional","affiliation":[{"name":"Hospital for Sick Children Toronto Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Timothy J.","family":"Bradley","sequence":"additional","affiliation":[{"name":"Hospital for Sick Children Toronto Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cameron","family":"Slorach","sequence":"additional","affiliation":[{"name":"Hospital for Sick Children Toronto Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John A.","family":"Reynolds","sequence":"additional","affiliation":[{"name":"National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH Bethesda Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarfaraz","family":"Hasni","sequence":"additional","affiliation":[{"name":"National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH Bethesda Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Becky","family":"Thompson","sequence":"additional","affiliation":[{"name":"University of Michigan Ann Arbor"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lawrence","family":"Ng","sequence":"additional","affiliation":[{"name":"Hospital for Sick Children Toronto Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deborah","family":"Levy","sequence":"additional","affiliation":[{"name":"Hospital for Sick Children Toronto Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Earl","family":"Silverman","sequence":"additional","affiliation":[{"name":"Hospital for Sick Children Toronto Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariana J.","family":"Kaplan","sequence":"additional","affiliation":[{"name":"National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH Bethesda Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2015,7,28]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1002\/1529-0131(200110)44:10<2331::AID-ART395>3.0.CO;2-I"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1080\/08916930903002479"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1097\/01.bor.0000137852.42270.0f"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.192639"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1186\/ar4212"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1136\/annrheumdis-2012-202315"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2003-09-3198"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2007-05-089086"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20021553"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa043814"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1002\/art.34504"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1001782"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0037000"},{"key":"e_1_2_7_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jpeds.2014.04.015"},{"key":"e_1_2_7_16_1","doi-asserted-by":"publisher","DOI":"10.2337\/dc12-1206"},{"key":"e_1_2_7_17_1","doi-asserted-by":"publisher","DOI":"10.1002\/art.1780400928"},{"key":"e_1_2_7_18_1","first-page":"1991","article-title":"Revision of the proposed classification criteria for juvenile idiopathic arthritis: Durban, 1997","volume":"25","author":"Petty RE","year":"1998","journal-title":"J Rheumatol"},{"key":"e_1_2_7_19_1","doi-asserted-by":"publisher","DOI":"10.1002\/art.1780350606"}],"container-title":["Arthritis &amp; 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