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リンパ球の脱出は,シモスおよび周辺リンパ性臓器からS1P受容体1に依存しています
Mehrdad Matloubian1, Charles G Lo, Guy Cinamon
1Howard Hughes Medical Institute and Department of Microbiology, University of California San Francisco, 513 Parnassus Avenue, San Francisco, California 94143-0414, USA.
Nature
|January 23, 2004
まとめ
スフィンゴシン-1-ホスファート受容体1 (S1P1) は,T細胞とB細胞の動きに不可欠です. この研究は,S1P1が,免疫細胞の密輸に不可欠な,胸腺およびリンパ性臓器からのリンパ球の脱出を制御することを明らかにしています.
科学分野:
- 免疫学 免疫学とは
- 細胞生物学 細胞生物学
- 分子生物学は分子生物学である.
背景:
- 適応免疫は,リンパ性臓器と組織間のリンパ球の循環に依存しています.
- リンパ性臓器からのリンパ細胞の脱出を制御するメカニズムは完全に理解されていません.
- 免疫抑制剤であるFTY720は,スフィンゴシン-1-フォスファート (S1P) 受容体と相互作用することによって,リンパ球の密輸に影響します.
研究 の 目的:
- S1P受容体,特にS1P受容体1 (S1P1) が,正常な免疫細胞取引における役割を調査する.
- リンパ球の脱出を制御するメカニズムを明らかにする 胸腺と二次リンパ性臓器からのリンパ球の脱出.
- 免疫抑制薬FTY720.0の作用メカニズムについて説明します.
主な方法:
- 造血細胞にS1P1が欠けているマウスを生成した.
- 養子細胞移植実験を行いました.
- 胸腺,血液,リンパ,リンパ性臓器のリンパ球群を分析した.
- リンパ球の発達と活性化中のS1P1発現と化学反応反応を研究した.
主要な成果:
- S1P1が欠けていたマウスは,胸膜出口の障害により,周辺のT細胞が完全に欠けていた.
- B細胞は血液とリンパに欠乏しており,S1P1の出血にS1P1の役割があることを示しています.
- S1P1は,リンパ性臓器からT細胞とB細胞の脱出に本質的に必要である.
- S1P1発現は,胸膜の退出前に上調され,外周活性化時に下調され,細胞保持と相関する.
- FTY720治療は,S1P1のダウンレギュレーションにより,リンパ球の封じ込めを引き起こし,これらの発見を模倣します.
結論:
- S1P1はリンパ球の再循環に不可欠です.
- S1P1は,胸腺と周辺リンパ性臓器の両方からリンパ球の脱出を調節する.
- S1P1の機能を理解することで,FTY720の免疫抑制のメカニズムを明らかにし,免疫細胞の密輸制御のための戦略を伝えることができます.
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