| ○種別 (必須): | □ | 学術論文 (審査論文)
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| ○言語 (必須): | □ | 英語
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| ○招待 (推奨): |
| ○審査 (推奨): |
| ○カテゴリ (推奨): |
| ○共著種別 (推奨): |
| ○学究種別 (推奨): |
| ○組織 (推奨): | 1. | 徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.基礎歯学系.口腔分子病態学 (2015年4月1日〜)
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| ○著者 (必須): | 1. | (英) Kurosawa Mie (日) 黒澤 実愛 (読) くろさわ みえ
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| ○学籍番号 (推奨): | □ | ****
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| 2. | 新垣 理恵子
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| 3. | 山田 安希子
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| 4. | 常松 貴明 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.基礎歯学系.口腔分子病態学])
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| ○貢献度 (任意): |
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| 5. | 工藤 保誠 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.基礎歯学系.口腔生命科学])
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| 6. | (英) Sprent J (日) (読)
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| 7. | 石丸 直澄 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.基礎歯学系.口腔分子病態学])
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| ○題名 (必須): | □ | (英) NF κB2 Controls the Migratory Activity of Memory T Cells by Regulating Expression of CXCR4 in a Mouse Model of Sjögren's Syndrome (日)
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| ○副題 (任意): |
| ○要約 (任意): | □ | (英) Dysregulated chemokine signaling contributes to autoimmune diseases by facilitating aberrant T cell infiltration into target tissues, but the specific chemokines, receptors, and T cell populations remain largely unidentified. The aim of this study was to examine the role of the potent chemokine CXCL12 and its receptor CXCR4 in the T cell autoimmune response, using alymphoplasia (aly)/aly mice, a model of Sjögren's syndrome (SS). T cell phenotypes in the salivary gland of aly/aly mice were evaluated using immunologic analysis. An in vitro migration assay was used to assess T cell migratory activity toward several chemokines. Gene expression of chemokine receptors and transforming growth factor β receptors (TGFβRs) was measured by quantitative reverse transcription-polymerase chain reaction. The CXCR4 antagonist AMD3100 was administered to the aly/aly mice in order to evaluate its suppressive effect on autoimmune lesions. Effector memory T (TEM) cells derived from aly/aly mice demonstrated higher in vitro migratory activity toward CXCL12 than did TEM cells from aly/+ mice. CXCL12 expression was specifically up-regulated in the SS target cells of aly/aly mice. TEM cells from RelB mice, but not Nfkb1 mice, also showed high migratory activity toward CXCL12, implicating a role of the nonclassical RelB/NF-κB2 pathway in the regulation of TEM cell migration. TEM cells from aly/aly mice also overexpressed TGFβR type I (TGFβRI) and TGFβRII. The CXCR4 antagonist AMD3100 suppressed autoimmune lesions in aly/aly mice by reducing TEM cell infiltration. Our results suggest that the RelB/NF-κB2 pathway regulates T cell migration to autoimmune targets through TGFβ/TGFβR-dependent regulation of CXCL12/CXCR4 signaling. This suggests that these signaling pathways are potential therapeutic targets for the treatment of autoimmune diseases. (日)
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| ○キーワード (推奨): | 1. | (英) Animals (日) (読)
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| 2. | (英) Chemokine CXCL12 (日) (読)
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| 3. | (英) Chemotaxis, Leukocyte (日) (読)
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| 4. | (英) Disease Models, Animal (日) (読)
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| 5. | (英) Gene Expression Regulation (日) (読)
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| 6. | (英) In Vitro Techniques (日) (読)
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| 7. | (英) Mice (日) (読)
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| 8. | (英) Mice, Knockout (日) (読)
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| 9. | (英) NF-kappa B p52 Subunit (日) (読)
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| 10. | (英) Receptors, CXCR4 (日) (読)
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| 11. | (英) Sjogren's Syndrome (日) (読)
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| 12. | (英) T-Lymphocytes (日) (読)
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| 13. | (英) Transcription Factor RelB (日) (読)
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| ○発行所 (推奨): |
| ○誌名 (必須): | □ | Arthritis & Rheumatology (American College of Rheumatology)
(pISSN: 2326-5191, eISSN: 2326-5205)
| ○ISSN (任意): | □ | 2326-5205
ISSN: 2326-5191
(pISSN: 2326-5191, eISSN: 2326-5205) Title: Arthritis & rheumatology (Hoboken, N.J.)Title(ISO): Arthritis RheumatolSupplier: American College of RheumatologyPublisher: Wiley Publishing (NLM Catalog)
(Wiley)
(Scopus)
(CrossRef)
(Scopus information is found. [need login]) | [継承] |
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| ○巻 (必須): | □ | 69
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| ○号 (必須): | □ | 11
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| ○頁 (必須): | □ | 2193 2202
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| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2017年 11月 初日 (平成 29年 11月 初日)
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| ○URL (任意): |
| ○DOI (任意): | □ | 10.1002/art.40230 (→Scopusで検索)
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| ○PMID (任意): | □ | 28804991 (→Scopusで検索)
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| ○CRID (任意): |
| ○WOS (任意): |
| ○Scopus (任意): | □ | 2-s2.0-85031674261
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| ○指導教員 (推奨): |
| ○備考 (任意): | 1. | (英) Article.ELocationID: 10.1002/art.40230 (日)
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| 2. | (英) Article.PublicationTypeList.PublicationType: Journal Article (日)
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| 3. | (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't (日)
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