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In this study, we investigated whether a local increase in interleukin IL-17 in keloid tissues stimulates the production of stromal cell\u2013derived factor-1 (SDF-1) in KFs causing further recruitment of IL-17-producing T helper 17 (Th17) cells, which subsequently creates a positive feedback loop. Histological assessment was performed and the change in the expression of IL-17, IL-1\u03b2, IL-6, and TNF-\u03b1 which of fibrosis and inflammation associated markers was examined. In addition, fibroblasts were treated with IL-17 in the presence or absence of STAT3 inhibitor STA-21; SDF-1 levels and fibrosis genes were measured. Our results showed that fibrotic reaction and expression of proinflammatory cytokines including IL-17 were most prominent in the growing margin (perilesional area) of keloid tissue and Th17 cells significantly infiltrated the perilesional area. In addition, IL-17 upregulated the expression of SDF-1, collagen, and \u03b1-SMA in KFs. Finally, STA-21 decreased SDF-1\u03b1 expression and the expression of fibrosis genes in KFs even after IL-17 stimulation. Our study demonstrated that a local increase in IL-17 in keloid tissues stimulates the production of SDF-1 in KFs causing further recruitment of IL-17-producing T helper 17 (Th17) cells, which subsequently creates a positive feedback loop. These findings suggest that STAT3 inhibition can be used to treat keloid scars by reversing the vicious cycle between Th17 cells and KFs.<\/jats:p>","DOI":"10.1007\/s10753-019-01148-1","type":"journal-article","created":{"date-parts":[[2019,12,9]],"date-time":"2019-12-09T04:29:13Z","timestamp":1575865753000},"page":"664-672","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":52,"title":["IL-17 Induced Stromal Cell\u2013Derived Factor-1 and Profibrotic Factor in Keloid-Derived Skin Fibroblasts via the STAT3 Pathway"],"prefix":"10.1007","volume":"43","author":[{"given":"Seon-Yeong","family":"Lee","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eun Kyung","family":"Kim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hyun Beom","family":"Seo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeong Won","family":"Choi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jin Hee","family":"Yoo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kyoung Ah","family":"Jung","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Da-Som","family":"Kim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seung Cheon","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Soo Jin","family":"Moon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jung Ho","family":"Lee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5715-3989","authenticated-orcid":false,"given":"Mi-La","family":"Cho","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2019,12,9]]},"reference":[{"issue":"1","key":"1148_CR1","doi-asserted-by":"publisher","first-page":"122","DOI":"10.1111\/j.1524-475X.2006.00193.x","volume":"15","author":"VC Sandulache","year":"2007","unstructured":"Sandulache, V.C., A. Parekh, H. Li-Korotky, J.E. Dohar, and P.A. Hebda. 2007. Prostaglandin E2 inhibition of keloid fibroblast migration, contraction, and transforming growth factor (TGF)-beta1-induced collagen synthesis. Wound Repair and Regeneration 15 (1): 122\u2013133.","journal-title":"Wound Repair and Regeneration"},{"issue":"6","key":"1148_CR2","doi-asserted-by":"publisher","first-page":"833","DOI":"10.3892\/br.2013.169","volume":"1","author":"X Dong","year":"2013","unstructured":"Dong, X., S. Mao, and H. Wen. 2013. Upregulation of proinflammatory genes in skin lesions may be the cause of keloid formation (review). Biomedical Reports 1 (6): 833\u2013836.","journal-title":"Biomedical Reports"},{"issue":"34 Suppl","key":"1148_CR3","first-page":"14","volume":"100 (5)","author":"L Lei","year":"2016","unstructured":"Lei, L., C. Zhao, F. Qin, Z.Y. He, X. Wang, and X.N. Zhong. 2016. 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