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著作: [石丸 直澄]/[新田 剛]/[新垣 理恵子]/[山田 安希子]/Lipp Martin/[高浜 洋介]/[林 良夫]/In situ Patrolling of Regulatory T cells is Essential for Protecting Autoimmune Exocrinopathy/[PLoS ONE]

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EID
203547
EOID
657314
Map
0
LastModified
2012年9月3日(月) 15:12:09
Operator
大家 隆弘
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TRUE
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Owner
福井 仁美
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種別 必須 学術論文(審査論文)
言語 必須 英語
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
著者 必須
  1. 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])
    役割 任意
    貢献度 任意
    学籍番号 推奨
  2. 新田 剛
    役割 任意
    貢献度 任意
    学籍番号 推奨
  3. 新垣 理恵子([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])
    役割 任意
    貢献度 任意
    学籍番号 推奨
  4. 山田 安希子
    役割 任意
    貢献度 任意
    学籍番号 推奨
  5. (英) Lipp Martin
    役割 任意
    貢献度 任意
    学籍番号 推奨
  6. 高浜 洋介
    役割 任意
    貢献度 任意
    学籍番号 推奨
  7. 林 良夫
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    貢献度 任意
    学籍番号 推奨
題名 必須

(英) In situ Patrolling of Regulatory T cells is Essential for Protecting Autoimmune Exocrinopathy

副題 任意
要約 任意

(英) Migration of T cells, including regulatory T (Treg) cells, into the secondary lymph organs is critically controlled by chemokines and adhesion molecules. However, the mechanisms by which Treg cells regulate organ-specific autoimmunity via these molecules remain unclear. Although we previously reported autoimmune exocrinopathy resembling Sjögren's syndrome (SS) in the lacrimal and salivary glands from C-C chemokine receptor 7 (CCR7)-deficient mice, it is still unclear whether CCR7 signaling might specifically affect the dynamics and functions of Treg cells in vivo. We therefore investigated the cellular mechanism for suppressive function of Treg cells via CCR7 in autoimmunity using mouse models and human samples. Patrolling Treg cells were detected in the exocrine organs such as lacrimal and salivary glands from normal mice that tend to be targets for autoimmunity while the Treg cells were almost undetectable in the exocrine glands of CCR7(-/-) mice. In addition, we found the significantly increased retention of CD4(+)CD25(+)Foxp3(+) Treg cells in the lymph nodes of CCR7(-/-) mice with aging. Although Treg cell egress requires sphingosine 1-phosphate (S1P), chemotactic function to S1P of CCR7-/- Treg cells was impaired compared with that of WT Treg cells. Moreover, the in vivo suppression activity was remarkably diminished in CCR7(-/-) Treg cells in the model where Treg cells were co-transferred with CCR7(-/-) CD25(-)CD4(+) T cells into Rag2(-/-) mice. Finally, confocal analysis showed that CCR7(+)Treg cells were detectable in normal salivary glands while the number of CCR7(+)Treg cells was extremely decreased in the tissues from patients with Sjögren's syndrome. These results indicate that CCR7 essentially governs the patrolling functions of Treg cells by controlling the traffic to the exocrine organs for protecting autoimmunity. Characterization of this cellular mechanism could have clinical implications by supporting development of new diagnosis or treatments for the organ-specific autoimmune diseases such as Sjögren's syndrome and clarifying how the local immune system regulates autoimmunity.

キーワード 推奨
  1. (英) Animals
  2. (英) Autoimmune Diseases
  3. (英) Cell Movement
  4. (英) Exocrine Glands
  5. (英) Lymphoid Tissue
  6. (英) Mice
  7. (英) Mice, Knockout
  8. (英) Receptors, CCR7
  9. (英) T-Lymphocytes, Regulatory
発行所 推奨 (英) Public Library of science-Author Billing
誌名 必須 PLoS ONE(Public Library of Science)
(eISSN: 1932-6203)
ISSN 任意 1932-6203
ISSN: 1932-6203 (eISSN: 1932-6203)
Title: PloS one
Title(ISO): PLoS One
Publisher: Public Library of Science
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
必須 5
必須 1
必須 e8588 e8588
都市 任意
年月日 必須 2010年 1月 5日
URL 任意
DOI 任意 10.1371/journal.pone.0008588    (→Scopusで検索)
PMID 任意 20052419    (→Scopusで検索)
NAID 任意
WOS 任意
Scopus 任意
評価値 任意
被引用数 任意
指導教員 推奨
備考 任意
  1. (英) Article.Affiliation: Department of Oral Molecular Pathology, Institute of Health Biosciences, The University of Tokushima Graduate School, Kuramotocho, Tokushima, Japan.

  2. (英) Article.PublicationTypeList.PublicationType: Journal Article

  3. (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't

  4. (英) OtherID: PMC2798967