{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T03:46:25Z","timestamp":1791171985073,"version":"4.1.0"},"reference-count":42,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2011,6,1]],"date-time":"2011-06-01T00:00:00Z","timestamp":1306886400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2011,6,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>TGF-\u03b2 is required for both Foxp3+ regulatory T cell (Treg) and Th17 commitment. Plasmacytoid DCs (pDC) have been shown to participate to both Treg and Th17 commitment as well. However, few studies have evaluated the direct effect of TGF-\u03b2 on pDC, and to our knowledge, no study has assessed the capacity of TGF-\u03b2\u2013exposed pDC to polarize naive CD4+ T cells. In this paper, we show that TGF-\u03b2\u2013treated pDC favor Th17 but not Treg commitment. This process involves a TGF-\u03b2\/Smad signal, because TGF-\u03b2 treatment induced Smad2 phosphorylation in pDC and blockade of TGF-\u03b2 signaling with the SD208 TGF-\u03b2RI kinase inhibitor abrogated Th17 commitment induced by TGF-\u03b2\u2013treated pDC. Moreover, TGF-\u03b2 mRNA synthesis and active TGF-\u03b2 release were induced in TGF-\u03b2\u2013treated pDC and anti\u2013TGF-\u03b2 Ab blocked Th17 commitment. Unexpectedly, TGF-\u03b2 treatment also induced increased IL-6 production by pDC, which serves as the other arm for Th17 commitment driven by TGF-\u03b2\u2013exposed pDC, because elimination of IL-6\u2013mediated signal with either IL-6\u2013 or IL-6R\u03b1\u2013specific Abs prevented Th17 commitment. The in vivo pathogenic role of TGF-\u03b2\u2013treated pDC was further confirmed in the Th17-dependent collagen-induced arthritis model in which TGF-\u03b2\u2013treated pDC injection significantly increased arthritis severity and pathogenic Th17 cell accumulation in the draining lymph nodes. Thus, our data reveal a previously unrecognized effect of TGF-\u03b2\u2013rich environment on pDC ability to trigger Th17 commitment. Such findings have implications in the pathogenesis of autoimmune diseases or immune responses against mucosal extracellular pathogens.<\/jats:p>","DOI":"10.4049\/jimmunol.1002497","type":"journal-article","created":{"date-parts":[[2011,4,26]],"date-time":"2011-04-26T03:29:30Z","timestamp":1303788570000},"page":"6157-6164","source":"Crossref","is-referenced-by-count":53,"title":["TGF-\u03b2\u2013Exposed Plasmacytoid Dendritic Cells Participate in Th17 Commitment"],"prefix":"10.1093","volume":"186","author":[{"given":"Francis","family":"Bonnefoy","sequence":"first","affiliation":[{"name":"INSERM, Unit\u00e9 Mixte de Recherche 645 , F-25020 Besan\u00e7on Cedex ,","place":["France"]},{"name":"Universit\u00e9 de Franche-Comt\u00e9, Institut F\u00e9d\u00e9ratif de Recherche 133 , F-25020 Besan\u00e7on Cedex ,","place":["France"]},{"name":"Etablissement Fran\u00e7ais du Sang de Bourgogne Franche-Comt\u00e9 , F-25020 Besan\u00e7on Cedex 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