{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T18:31:47Z","timestamp":1791311507005,"version":"4.3.1"},"reference-count":52,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2010,3,1]],"date-time":"2010-03-01T00:00:00Z","timestamp":1267401600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AR056099"],"award-info":[{"award-number":["AR056099"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AR055240"],"award-info":[{"award-number":["AR055240"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AR048269"],"award-info":[{"award-number":["AR048269"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["NS34510"],"award-info":[{"award-number":["NS34510"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2010,3,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Angiogenesis is an early and a critical event in the pathogenesis of rheumatoid arthritis (RA). Neovascularization is dependent on endothelial cell activation, migration and proliferation, and inhibition of angiogenesis may provide a novel therapeutic approach in RA. In this study, we document a novel role of IL-17 in mediating angiogenesis. Local expression of IL-17 in mouse ankles increases vascularity. We further demonstrate that IL-17 is angiogenic by showing its ability to promote blood vessel growth in Matrigel plugs in vivo. Additionally, IL-17, in concentrations present in the RA joint, induces human lung microvascular endothelial cell (HMVEC) migration mediated through the PI3K\/AKT1 pathway. Furthermore, suppression of the PI3K pathway markedly reduces IL-17\u2013induced tube formation. We also show that both IL-17\u2013induced HMVEC chemotaxis and tube formation are mediated primarily through IL-17 receptor C. Neutralization of either IL-17 in RA synovial fluids or IL-17 receptor C on HMVECs significantly reduces the induction of HMVEC migration by RA synovial fluid. Finally, RA synovial fluid immunoneutralized with anti\u2013IL-17 and antivascular endothelial growth factor does not reduce HMVEC migration beyond the effect detected by immunodepleting each factor alone. These observations identify a novel function for IL-17 as an angiogenic mediator in RA, supporting IL-17 as a therapeutic target in RA.<\/jats:p>","DOI":"10.4049\/jimmunol.0903271","type":"journal-article","created":{"date-parts":[[2010,2,19]],"date-time":"2010-02-19T21:41:20Z","timestamp":1266615680000},"page":"3233-3241","source":"Crossref","is-referenced-by-count":163,"title":["IL-17 Contributes to Angiogenesis in Rheumatoid Arthritis"],"prefix":"10.1093","volume":"184","author":[{"given":"Sarah R","family":"Pickens","sequence":"first","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael V","family":"Volin","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Chicago College of Osteopathic Medicine, Midwestern University , Downers Grove, IL 60515"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"II","given":"Arthur M","family":"Mandelin","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jay K","family":"Kolls","sequence":"additional","affiliation":[{"name":"Department of Genetics, Louisiana State University Health Sciences Center , New Orleans, LA 70112"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard M","family":"Pope","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University"},{"name":"Jesse Brown Veterans Affairs Hospitals, Chicago Healthcare System , Chicago, IL 60611"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shiva","family":"Shahrara","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2010,3,15]]},"reference":[{"key":"2026012806343389900_r1","doi-asserted-by":"crossref","first-page":"337","DOI":"10.1038\/nri2295","article-title":"TH17 cells in development: an updated view of their molecular identity and genetic programming.","volume":"8","author":"Dong","year":"2008","journal-title":"Nat. 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