転写因子Gata6は,組織マクロファージのフェノタイプと増殖的再生を結びつける

Marcela Rosas¹, Luke C Davies¹, Peter J Giles²

¹Cardiff Institute of Infection and Immunity, Cardiff University School of Medicine, Heath Park, Cardiff, CF14 4XN, UK.

Science (New York, N.Y.)

|April 26, 2014

まとめ

腹膜のマクロファージのような組織に居住するマクロファージは,自己再生と適切な機能のためにGata6遺伝子に依存しています. Gata6の喪失はマクロファージの増殖を阻害し,炎症解消を遅らせます.

科学分野:

免疫学免疫学とは
細胞生物学細胞生物学
トランスクリプトミクス (Transcriptomics) とは

背景:

組織在住マクロファージは,ニッチ特有の機能により異質性を示す.
多くのマクロファージの集団は,成人の骨髄とは独立して自己再生しますが,そのメカニズムは不明です.

研究の目的:

組織在住マクロファージの自己再生を制御する分子機構を特定する.
腹腔内マクロファージの生物学における転写因子Gata6の役割を調査する.

主な方法:

マウスの腹腔内マクロファージの転写プロファイリング.
ミエロイド細胞に選択的なGata6欠乏症を生成するための遺伝子操作.
マクロファージの増殖と炎症反応の分析.

主要な成果:

腹腔内マクロファージは,転写因子 Gata6 を発現する主要な自己再生集団として特定されました.
ミエロイド細胞の選択的なGata6欠乏症は,腹腔内マクロファージトランスクリプトームを変化させた.
Gata6欠乏症はマクロファージの増殖を制御不能にし,炎症解消を遅らせました.

結論:

組織マクロファージのフェノタイプは,組織選択的転写調節によって制御されます.
転写因子Gata6は,腹腔内マクロファージの増殖的な再生に不可欠です.
マクロファージ増殖の Gata6 調節は,炎症解消と関連しています.

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