Abrogation of Rbpj attenuates experimental autoimmune uveoretinitis by inhibiting IL-22-producing CD4+ T cells 2

• Material Type: 博士論文
• ISSN: 1932-6203
• Title: Abrogation of Rbpj attenuates experimental autoimmune uveoretinitis by inhibiting IL-22-producing CD4+ T cells
• Volume: 9 2
• Author/Editor: Bhuyan, Zaied Ahmed; Asanoma, Michihito; Iwata, Akiko; Ishifune, Chieko; Maekawa, Yoichi; Shimada, Mitsuo; Yasutomo, Koji
• Author Heading: Bhuyan, Zaied Ahmed; Asanoma, Michihito; Iwata, Akiko; Ishifune, Chieko; Maekawa, Yoichi; Shimada, Mitsuo; Yasutomo, Koji
• Publication, Distribution, etc.: PLOS
• Publication Date: 2014-02-28
• Publication Date (W3CDTF): 2014-02-28
• Alternative Title: Rbpjの欠損はCD4陽性T細胞によるIL-22産生を抑制することで実験的自己免疫性網膜ブドウ膜炎の症状を軽減させる; Abrogation of Rbpj attenuates uveoretinitis
• Periodical title: PLOS ONE
• Degree grantor/type: 徳島大学
• Date Granted: 2014-03-19
• Date Granted (W3CDTF): 2014-03-19
• Dissertation Number: 甲第2740号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第2740号
• Text Language Code: eng
• Subject Heading: Notch; Rbpj; EAU (Experimental Autoimmune Uveoretinitis); GSI (γ secretase inhibitor); IL-22
• Target Audience: 一般
• Note (General): Experimental autoimmune uveoretinitis (EAU) is an organ-specific T cell-mediated disease induced by immunizing mice with interphotoreceptor retinoid binding protein (IRBP). Autoaggressive CD4+ T cells are the major pathogenic population for EAU. We investigated the contribution of Notch signaling in T cells to EAU pathogenesis because Notch signaling regulates various aspects of CD4+ T cell functions. Rbpj is required for Notch signaling, and Rbpj deficiency in T cells inhibited EAU disease severity. The amelioration of EAU in T cell-specific Rbpj-deficient mice correlated with low levels of IL-22 production from CD4+ T cells, although IRBP-specific CD4+ T cell proliferation and Th17 differentiation were unaffected. Administration of recombinant IL-22 during the late phase, but not the early phase, of EAU increased EAU clinical scores in T cell-specific Rbpj-deficient mice. Notch inhibition in mice immunized with IRBP with a γ-secretase inhibitor (GSI) suppressed EAU progression, even when GSI was administered as late as 13 days after IRBP immunization. Our data demonstrate that Rbpj/Notch-mediated IL-22 production in T cells has a key pathological role in the late phase of EAU, and suggest that Notch blockade might be a useful therapeutic approach for treating EAU.
• DOI: info:doi/10.1371/journal.pone.0089266; https://doi.org/info:doi/10.1371/journal.pone.0089266
• Persistent ID (NDL): info:ndljp/pid/9984259; https://dl.ndl.go.jp/pid/9984259
• Collection: 障害者向け資料
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• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2016-06-03T01:05:16+09:00
• Format (IMT): application/pdf
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• Periodical Title (URI): http://repo.lib.tokushima-u.ac.jp/106133
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp