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We examined the role of Wnt5a signaling in intestinal immunity using conditional knockout mice for Wnt5a and its receptor Ror2. Removing Wnt5a or Ror2 in adult mice suppressed dextran sodium sulfate (DSS)-induced colitis. It also attenuated the DSS-dependent increase in inflammatory cytokine production and decreased interferon-\u03b3 (IFN-\u03b3)-producing CD4<jats:sup>+<\/jats:sup> Th<jats:sub>1<\/jats:sub> cell numbers in the colon. Wnt5a was highly expressed in stromal fibroblasts in ulcerative lesions in the DSS-treated mice and inflammatory bowel disease patients. Dendritic cells (DCs) isolated from the colon of <jats:italic>Wnt5a<\/jats:italic> and <jats:italic>Ror2<\/jats:italic> deficient mice reduced the ability to differentiate na\u00efve CD4<jats:sup>+<\/jats:sup> T cells to IFN-\u03b3-producing CD4<jats:sup>+<\/jats:sup> Th<jats:sub>1<\/jats:sub> cells. <jats:italic>In vitro<\/jats:italic> experiments demonstrated that the Wnt5a-Ror2 signaling axis augmented the DCs priming effect of IFN-\u03b3, leading to enhanced lipopolysaccharide (LPS)-induced interleukin (IL)-12 expression. Taken together, these results suggest that Wnt5a promotes IFN-\u03b3 signaling, leading to IL-12 expression in DCs and thereby inducing Th<jats:sub>1<\/jats:sub> differentiation in colitis.<\/jats:p>","DOI":"10.1038\/srep10536","type":"journal-article","created":{"date-parts":[[2015,6,1]],"date-time":"2015-06-01T19:19:33Z","timestamp":1433186373000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":65,"title":["The Wnt5a-Ror2 axis promotes the signaling circuit between interleukin-12 and interferon-\u03b3 in colitis"],"prefix":"10.1038","volume":"5","author":[{"given":"Akira","family":"Sato","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hisako","family":"Kayama","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kensaku","family":"Shojima","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shinji","family":"Matsumoto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hirofumi","family":"Koyama","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasuhiro","family":"Minami","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Satoshi","family":"Nojima","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eiichi","family":"Morii","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroaki","family":"Honda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kiyoshi","family":"Takeda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akira","family":"Kikuchi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2015,6,1]]},"reference":[{"key":"BFsrep10536_CR1","doi-asserted-by":"publisher","first-page":"17","DOI":"10.1111\/j.1748-1716.2011.02294.x","volume":"204","author":"A Kikuchi","year":"2012","unstructured":"Kikuchi, A., Yamamoto, H., Sato, A. & Matsumoto, S. 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