CD5L/AIM 脂質生物合成を調節し,Th17細胞の病原性を抑制する
Chao Wang1, Nir Yosef2, Jellert Gaublomme3
1Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Cell
|November 27, 2015
まとめ
CD5L/ AIMタンパク質はTヘルパー17 (Th17) 細胞の病原性を調節し,自己免疫を予防する. CD5Lの損失は,非病原性Th17細胞を病原性細胞に変換し,脂質代謝を変化させます.
科学分野:
- 免疫学
- 細胞生物学
- 代謝経路
背景:
- Tヘルパー17 (Th17) 細胞は免疫に不可欠ですが,自己免疫疾患を引き起こす可能性があります.
- 病原性対非病原性Th17細胞状態を制御するメカニズムは完全に理解されていません.
研究 の 目的:
- 病原性と非病原性Th17細胞サブセットを区別する重要なレギュレータを特定する.
- Th17細胞の病原性を調節するCD5L/AIMの機能的役割を解明する.
主な方法:
- 単細胞RNAシーケンシング (scRNA-seq) で,差異的な遺伝子発現を特定する.
- Th17細胞の病原性に対するCD5Lのインパクトを in vivoで評価するための機能検査
- 細胞内脂質代謝と転写因子の活性分析
主要な成果:
- CD5L/AIMは,非病原性Th17細胞のマーカーとして特定され,病原性サブセットには含まれていません.
- CD5L欠乏症は,非病原性Th17細胞を病原性自己免疫フェノタイプに変換した.
- CD5Lは細胞内脂質群を調節し,コレステロールの生物合成とRorγt活性に影響を与え,Th17の病原性を調節する.
結論:
- CD5L/AIMは,Th17細胞の病原性を制御する重要なスイッチとして機能する.
- 脂質代謝は,Th17細胞による免疫反応と自己免疫疾患のバランスをとる上で重要な決定因子です.
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