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  1. 30 医学部・医学研究科・保健学研究科
  2. 30b 弘前医学 = Hirosaki Medical Journal
  3. 59巻Supplement

NK-activating dendritic cells are elicited by stimulation with Toll-like receptor 3

http://hdl.handle.net/10129/2215
http://hdl.handle.net/10129/2215
c3b679fd-099c-4563-8061-cf1cc7bb6967
名前 / ファイル ライセンス アクション
HirosakiMedJ_59_S43.pdf HirosakiMedJ_59_S43.pdf (1.3 MB)
Item type 学術雑誌論文 / Journal Article(1)
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

Seya, Tsukasa

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Matsumoto, Misako

× Matsumoto, Misako

Matsumoto, Misako

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Ebihara, Takashi

× Ebihara, Takashi

Ebihara, Takashi

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Akazawa, Takashi

× Akazawa, Takashi

Akazawa, Takashi

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著者所属
値 Department of Microbiology and Immunology, Hokkaido University Graduate School of Medicine
著者所属
値 Department of Microbiology and Immunology, Hokkaido University Graduate School of Medicine
著者所属
値 Department of Microbiology and Immunology, Hokkaido University Graduate School of Medicine
著者所属
値 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
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
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
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