CD8+ T細胞の宿命コミットメントにおける幹細胞性の表遺伝子制御
Luigia Pace1,2,3, Christel Goudot4,2, Elina Zueva4,2
1Institut Curie, PSL Research University, F-75005 Paris, France. luigia.pace@iigm.it genevieve.almouzni@curie.fr sebastian.amigorena@curie.fr.
Science (New York, N.Y.)
|January 13, 2018
まとめ
ヒストンメチルトランスフェラーゼSuv39h1は,CD8+T細胞における幹/記憶遺伝子を静止させます. 持続的な生存と記憶の再プログラムを促進し,エフェクターT細胞の分化における重要な役割を明らかにします.
科学分野:
- 免疫学
- エピジェネティクス
- 細胞生物学
背景:
- ネイヴなCD8+Tリンパ球は,異なる転写プログラムを持つ記憶細胞またはエフェクタ細胞に微分化します.
- T細胞系統の特異化中に遺伝子発現を制御するクロマチンダイナミクスの役割は完全に理解されていません.
研究 の 目的:
- CD8+ T細胞の分化中の遺伝子静止におけるヒストンメチルトランスファーゼ Suv39h1の機能を調査する.
- クロマチンの動態と遺伝子発現プログラムに対するSuv39h1の影響を明らかにする.
主な方法:
- Listeria monocytogenesの感染後に活性化されたマウンのCD8+T細胞を使用した.
- 遺伝子発現パターンを分析するために単細胞RNA配列を解析した.
- Suv39h1依存ヒストンH3ライシン9トリメチル化の役割を評価した.
主要な成果:
- Suv39h1依存のH3K9トリメチル化は,CD8+T細胞における幹細胞関連記憶遺伝子を調節する.
- Suv39h1欠乏したT細胞は,幹/記憶遺伝子の静止が損なわれている.
- Suv39h1の欠如は,CD8+ T細胞の生存率と長期記憶の可能性を高めます.
結論:
- Suv39h1は,CD8+ Tエフェクターの末端分化中に染色体マーキングによる幹/記憶遺伝子の静止化に不可欠である.
- Suv39h1媒介による遺伝子静止は,記憶ではなく,エフェクタルの運命への適切な進行を保証する.
- Suv39h1を標的にすると,T細胞の記憶の発達と免疫反応に影響する可能性があります.
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