乱交した脂質結合タンパク質は,トール型の受容体信号伝導のサブセルラー部位を多様化する

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Kevin S Bonham¹, Megan H Orzalli², Kachiko Hayashi³

¹Division of Gastroenterology, Boston Children's Hospital and Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.

|February 18, 2014

まとめ

トール型受容体 (TLR) は,細胞の様々な部位から信号を送る. アダプタタンパク質であるTIRAPは,異なる脂質に結合することで,TLRがプラズマ膜とエンドソームから免疫反応を活性化させることを可能にします.

科学分野:

免疫学免疫学とは
細胞生物学細胞生物学

背景:

トール型受容体 (TLR) は,先天性免疫システムの重要な構成要素です.
TLRは異なる臓器細胞に存在するが,共通の信号伝達経路に収束する.
TLRがさまざまな場所からどのように共通の経路を活性化するかは,まだ十分に理解されていません.

研究の目的:

TLRsが複数のサブセルラー位置から共通のシグナル伝達経路を活性化するメカニズムを調査する.
TLRシグナリング規制におけるソートアダプタTIRAPの役割を特定する.

主な方法:

TLRシグナリングの規制におけるTIRAPの機能を調査した.
TIRAPとフォスフォニノシチドの相互作用とその局所化を調べました.
ミドゾーム複合体の構成と,そのサイトカイン発現における役割を分析した.

主要な成果:

TIRAPは,プラズマ膜とエンドソームの両方からのTLRシグナリングを調節する.
TIRAPに依存するミドソーム組成は,炎症性サイトカイン発現に不可欠です.
TIRAPの乱交的なフォスホイノシチド結合ドメインにより,活性化されたTLRを複数の細胞区画で調査することができます.

結論:

TIRAPの脂質結合ドメインのプロムシキュイティは,多様なサブセルラー部位からのTLR信号伝導を促進します.
このメカニズムは,さまざまなTLR局所化にもかかわらず,効果的な先天的な免疫反応を可能にします.
この発見は,先天性免疫シグナリングの適応性についての洞察を提供します.

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