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However, its significance in clinical stratification and contribution to deterioration still need to be better understood.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>For hypothesis generation, we performed single\u2010cell RNA sequencing (scRNA\u2010seq) on skin biopsies (four patients with SSc and two controls) using the BD Rhapsody platform. Two publicly available data sets of skin scRNA\u2010seq were used for validation (GSE138669: 12 patients with diffuse cutaneous SSc [dcSSc] and 10 controls; GSE195452: 52 patients with dcSSc and 41 patients with limited cutaneous SSc [lcSSc] and 54 controls). The IFN\u20101 signature was mapped, functionally investigated in a bleomycin plus IFN\u03b1\u20102 adenovirus\u2010associated virus (AAV)\u2013induced model and verified in an SSc cohort (n\u00a0=\u00a061).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The discovery and validation data sets showed similar findings. Endothelial cells (ECs) had the most prominent IFN\u20101 signature among dermal nonimmune cells. The EC IFN\u20101 signature was increased both in patients with SSc versus controls and in patients with dcSSc versus those with lcSSc. Among EC subclusters, the IFN\u20101 signature was statistically higher in the capillary ECs of patients with dcSSc, which was higher than those in patients with lcSSc, which in turn was higher than those in healthy controls (HCs). Endothelial\u2010to\u2010mesenchymal transition (EndoMT) scores increased in parallel. Deteriorated bleomycin\u2010induced dermal fibrosis, EndoMT, and perivascular fibrosis and caused blood vessel loss with EC apoptosis. Vascular myxovirus resistance (MX) 1, an IFN\u20101 response protein, was significantly increased both in total SSc versus HC skin and in dcSSc versus lcSSc skin. Baseline vascular MX1 performed similarly to skin score in predicting disease progression over 6 to 34 months in total SSc and was superior in the dcSSc subpopulation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The EC IFN\u20101 signature distinguished SSc skin subtypes and disease progression and may contribute to vasculopathy and fibrosis.\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/art42662-toc-0001-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p><\/jats:sec>","DOI":"10.1002\/art.42662","type":"journal-article","created":{"date-parts":[[2023,7,25]],"date-time":"2023-07-25T01:42:07Z","timestamp":1690249327000},"page":"78-91","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["Endothelial Response to Type I Interferon Contributes to Vasculopathy and Fibrosis and Predicts Disease Progression of Systemic Sclerosis"],"prefix":"10.1002","volume":"76","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0706-3998","authenticated-orcid":false,"given":"Hanlin","family":"Yin","sequence":"first","affiliation":[{"name":"Department of Rheumatology Renji Hospital, Shanghai Jiao Tong University School of Medicine  Shanghai 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