{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T07:54:25Z","timestamp":1789631665357,"version":"build-2803163510"},"reference-count":40,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2026,4,23]],"date-time":"2026-04-23T00:00:00Z","timestamp":1776902400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,4,23]],"date-time":"2026-04-23T00:00:00Z","timestamp":1776902400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["acrjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Arthritis &amp;amp; Rheumatology"],"published-print":{"date-parts":[[2026,6]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>This study investigated the role of interleukin\u201017 (IL\u201017) in giant cell arteritis (GCA), which has remained uncertain despite previous research suggesting a contribution of Th17 cells to the disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Temporal artery biopsies (TABs) were cultured ex vivo in MATRIGEL with IL\u201017, secukinumab, or control IgG and subsequently analyzed using bulk RNA\u2010sequencing and real\u2010time quantitative polymerase chain reaction. Positive TABs with GCA features were compared to negative TABs or used to obtain in vitro cultures of myofibroblasts (MFs). Confocal microscopy analyzed IL\u201017 receptor expression. MFs and peripheral blood mononuclear cells cocultures were used to study T cell polarization.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Transcriptomic analysis showed that secukinumab treatment of positive TABs reduced expression of genes linked to vascular inflammation, notably\n                      <jats:italic>IL6<\/jats:italic>\n                      . Real\u2010time quantitative polymerase chain reaction analysis confirmed that secukinumab decreased messenger RNA encoding IL\u20106, CCL20, and granulocyte macrophage colony\u2010stimulating factor (GM\u2010CSF) in positive TABs, whereas IL\u201017 up\u2010regulated them in negative TABs. No changes were observed regarding the expression of genes related to vascular remodeling. IL\u201017 receptor chains were expressed on MFs, and their expression was enhanced by interferon\u2010\u03b3 (IFN\u2010\u03b3). Real\u2010time quantitative polymerase chain reaction and Luminex analyses confirmed IL\u201017\u2013driven upregulation of IL\u20106, CCL20, CCL2, GM\u2010CSF, and vascular endothelial growth factor (VEGF) in MFs, which was reversed by secukinumab. Addition of IFN\u2010\u03b3 to the culture increased the expression level of IL\u201017 receptor chains, resulting in a synergistic effect. Additionally, IL\u201017\u2013pretreated MFs promoted Th17 polarization.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>IL\u201017 exacerbates vascular inflammation in GCA by activating MFs and synergizing with IFN\u2010\u03b3 to increase production of proinflammatory cytokines (IL\u20106, GM\u2010CSF), chemokines (CCL20, CCL2), and angiogenic factors (VEGF), indicating that IL\u201017 is a key contributor to disease pathogenesis.<\/jats:p>\n                    <jats:p>\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/art70051-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/art.70051","type":"journal-article","created":{"date-parts":[[2026,1,12]],"date-time":"2026-01-12T14:42:59Z","timestamp":1768228979000},"page":"1268-1280","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["In Synergy With Interferon\u2010\u03b3, Interleukin\u201017 Activates Vascular Stromal Cells Toward a Proinflammatory Profile in Giant Cell Arteritis"],"prefix":"10.1002","volume":"78","author":[{"given":"H\u00e9l\u00e8ne","family":"Greigert","sequence":"first","affiliation":[{"name":"Department of Internal Medicine and Clinical Immunology, Referral Center for Rare Systemic Autoimmune and Autoinflammatory Diseases Dijon University Hospital, Universit\u00e9 EPE Bourgogne Europe  Dijon France"},{"name":"Department of Vascular Medicine Dijon University Hospital, Universit\u00e9 EPE Bourgogne Europe  Dijon France"},{"name":"Universit\u00e9 Marie et Louis Pasteur, EFS, INSERM UMR1098 RIGHT  Besan\u00e7on France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7289-7916","authenticated-orcid":false,"given":"Andr\u00e9","family":"Ramon","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Marie et Louis Pasteur, EFS, INSERM UMR1098 RIGHT  Besan\u00e7on France"},{"name":"Department of Rheumatology Dijon University Hospital, Universit\u00e9 EPE Bourgogne Europe  Dijon France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudie","family":"Cladiere","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Clinical Immunology, Referral Center for Rare Systemic Autoimmune and Autoinflammatory Diseases Dijon University Hospital, Universit\u00e9 EPE Bourgogne Europe  Dijon France"},{"name":"Universit\u00e9 Marie et Louis Pasteur, EFS, INSERM UMR1098 RIGHT  Besan\u00e7on France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Baptiste","family":"Lamarth\u00e9e","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Marie et Louis Pasteur, EFS, INSERM UMR1098 RIGHT  Besan\u00e7on France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Corentin","family":"Richard","sequence":"additional","affiliation":[{"name":"Unit of Molecular Biology, Department of Biology and Pathology of Tumors Georges\u2010Fran\u00e7ois Leclerc Cancer Center, Unicancer, ICMUB UMR CNRS 6302  Dijon France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marion","family":"Ciudad","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Clinical Immunology, Referral Center for Rare Systemic Autoimmune and Autoinflammatory Diseases Dijon University Hospital, Universit\u00e9 EPE Bourgogne Europe  Dijon France"},{"name":"Universit\u00e9 Marie et Louis Pasteur, EFS, INSERM UMR1098 RIGHT  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