論文

査読有り
2013年7月

D1-like dopamine receptors antagonist inhibits cutaneous immune reactions mediated by Th2 and mast cells

JOURNAL OF DERMATOLOGICAL SCIENCE
  • Tomoko Mori
  • Kenji Kabashima
  • Shoko Fukamachi
  • Etsushi Kuroda
  • Jun-ichi Sakabe
  • Miwa Kobayashi
  • Saeko Nakajima
  • Kazuhisa Nakano
  • Yoshiya Tanaka
  • Sho Matsushita
  • Motonobu Nakamura
  • Yoshiki Tokura
  • 全て表示

71
1
開始ページ
37
終了ページ
44
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.jdermsci.2013.03.008
出版者・発行元
ELSEVIER IRELAND LTD

Background: Dopamine transduces signals via five subtypes of G protein-coupled receptors. Among these subtypes, the D1 and D5 receptors belong to the D1-like group. Although dopamine is known to mediate immune responses, its involvement in cutaneous immunity remains unclear.
Objective: The aim of this study is to determine the role of dopamine and its D1-like receptors in cutaneous immune responses.
Methods: By using the D1-like receptor antagonist SCH 23390, we examined the role of D1-like receptors in murine models of Th1-type contact hypersensitivity and Th2-type atopic dermatitis in vivo, and in mast cells and Th2 cell differentiation in vitro.
Results: Administration of SCH 23390 did not affect Th1-type contact hypersensitivity but suppressed the immediate-type reaction (ITR) and the late phase reaction (LPR) in the atopic dermatitis model. In addition, SCH 23390-treated mice showed higher IFN-gamma and lower IL-4 mRNA levels in the ear skin of challenged mice than did non-treated mice as analyzed by real-time RT PCR. Consistently, the passive cutaneous anaphylaxis reaction was significantly reduced in SCH 23390-treated mice. Moreover, dopamine enhanced mast cell degranulation and Th2 cell differentiation, and both activities were abrogated by SCH 23390.
Conclusion: These findings suggest that the D1-like receptors mediate immediate and late phase skin reactions by promoting Th2 induction and mast cell degranulation. (C) 2013 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.jdermsci.2013.03.008
J-GLOBAL
https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201302293363210556
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000321681800005&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.jdermsci.2013.03.008
  • ISSN : 0923-1811
  • J-Global ID : 201302293363210556
  • Web of Science ID : WOS:000321681800005

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