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These\nreceptors are implicated in the differential screening of microbes by the host. Myeloid dendritic cells (mDCs)\nrecognize and respond to polyI:C, an analog of dsRNA, by endosomal TLR3 and cytoplasmic MDA5. NK cells are\ninduced in vivo by the administration of polyI:C to mice and in vitro are reciprocally activated by mDCs, although the\nmolecular mechanisms as yet undetermined. Here, we show that the TLR adapter TICAM-1 (TRIF) participates in\nmDC-derived antitumor NK activation. In a syngeneic mouse tumor implant model, intraperitoneal administration of\npolyI:C led to the retardation of tumor growth, which eff ect relied largely on NK activation. This NK-dependent tumor\nregression did not occur in TICAM-1-/- or IFNAR-/- mice, while a normal NK antitumor response was induced in PKR-/-,\nMyD88-/-, IFN-β-/- and wild-type mice. IFNAR was a prerequisite for the induction of IFN-α/β and TLR3. 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NK-activating dendritic cells are elicited by stimulation with Toll-like receptor 3
http://hdl.handle.net/10129/2215
http://hdl.handle.net/10129/2215c3b679fd-099c-4563-8061-cf1cc7bb6967
名前 / ファイル | ライセンス | アクション |
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HirosakiMedJ_59_S43.pdf (1.3 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2009-09-18 | |||||
タイトル | ||||||
タイトル | NK-activating dendritic cells are elicited by stimulation with Toll-like receptor 3 | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | natural killer cells (NK) | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | dendritic cells | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Toll-like receptor(TLR) | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | TICAM-1(TRIF) | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | adjuvant | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Seya, Tsukasa
× Seya, Tsukasa× Matsumoto, Misako× Ebihara, Takashi× Akazawa, Takashi |
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著者所属 | ||||||
Department of Microbiology and Immunology, Hokkaido University Graduate School of Medicine | ||||||
著者所属 | ||||||
Department of Microbiology and Immunology, Hokkaido University Graduate School of Medicine | ||||||
著者所属 | ||||||
Department of Microbiology and Immunology, Hokkaido University Graduate School of Medicine | ||||||
著者所属 | ||||||
Department of Immunology, Osaka Medical Center for Cancer and Cardiovascular Diseases | ||||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Double-stranded (ds)RNA-recognition receptors reside in the cytoplasm and membranes of cells. These receptors are implicated in the differential screening of microbes by the host. Myeloid dendritic cells (mDCs) recognize and respond to polyI:C, an analog of dsRNA, by endosomal TLR3 and cytoplasmic MDA5. NK cells are induced in vivo by the administration of polyI:C to mice and in vitro are reciprocally activated by mDCs, although the molecular mechanisms as yet undetermined. Here, we show that the TLR adapter TICAM-1 (TRIF) participates in mDC-derived antitumor NK activation. In a syngeneic mouse tumor implant model, intraperitoneal administration of polyI:C led to the retardation of tumor growth, which eff ect relied largely on NK activation. This NK-dependent tumor regression did not occur in TICAM-1-/- or IFNAR-/- mice, while a normal NK antitumor response was induced in PKR-/-, MyD88-/-, IFN-β-/- and wild-type mice. IFNAR was a prerequisite for the induction of IFN-α/β and TLR3. The lack of TICAM-1 did not aff ect IFN production but resulted in unresponsiveness to IL-12 production, mDC maturation and polyI:C-mediated antitumor activity. This NK activation required NK-mDC contact in in vitro transwell analysis. NKantitumor activity was successfully introduced into tumor-implanted mice by transferring mDCs expressing TICAM-1. Implanted tumor growth in IFNAR-/- mice was retarded by adoptively transferring polyI:C-treated TICACM-1-positive mDCs but not TICAM-1-/- mDCs. Thus, TICAM-1 rather than MDA5 in mDCs critically facilitated mDC-NK contact and activation of antitumor NK, resulting in the regression of low MHC-expressing tumors |
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引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 弘前医学. 59(Suppl.), 2007, p.S43-S51 | |||||
書誌情報 |
弘前医学 巻 59, 号 Supplement, p. S43-S51, 発行日 2007-11-29 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0439-1721 | |||||
書誌レコードID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AN00211444 | |||||
フォーマット | ||||||
内容記述タイプ | Other | |||||
内容記述 | application/pdf | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
日本十進分類法 | ||||||
主題Scheme | NDC | |||||
主題 | 494.5 | |||||
NIIサブジェクト | ||||||
主題Scheme | Other | |||||
主題 | 外科系臨床医学 | |||||
出版者 | ||||||
出版者 | 弘前大学大学院医学研究科・弘前医学会 | |||||
資源タイプ | ||||||
値 | Article |