dendritic 細胞による L-Myc 発現は,最適な T 細胞プライミングのために必要です
Wumesh KC1, Ansuman T Satpathy1, Aaron S Rapaport1
1Department of Pathology and Immunology, Washington University School of Medicine, 660 S. Euclid Avenue, St Louis, Missouri 63110, USA.
Nature
|February 11, 2014
まとめ
転写因子L-Myc (Mycl1によってエンコードされる) は, dendritic 細胞の発達と機能に不可欠です. L-Mycの損失は,感染中にT細胞のプライミングを損なっており,免疫反応におけるその役割を強調しています.
科学分野:
- 免疫学 免疫学とは
- 分子生物学は分子生物学である.
- 発達生物学 発達生物学について
背景:
- c-MycとN-Mycは,細胞の成長と胚の発達の主な調節体である.
- 関連する転写因子L-Myc (Mycl1によってコードされる) のin vivo,特に免疫系における役割は不明のままである.
- Mycファミリーのパラログ機能を理解することは,細胞の調節を解読するために不可欠です.
研究 の 目的:
- マウスにおけるL-Myc (Mycl1) のインビボ機能を調査する.
- 免疫細胞におけるL-Mycの発現パターンと調節機構を決定する.
- L-Myc欠乏がデンドリット細胞の発達とT細胞の免疫反応に与える影響を評価する.
主な方法:
- L-Mycの発現と機能を追跡するためのMycl1 ((gfp) レポーターマウスモデルの生成.
- 発達の過程と炎症信号への反応において, dendritic 細胞のサブセットにおける L-Myc 発現の分析.
- Mycl1欠乏マウスにおけるデンドリット細胞集団のフェノタイプ的特徴.
- 微生物感染症中のT細胞プライミング in vivoの評価.
主要な成果:
- L-Mycは,デンドリット細胞 (DC) で選択的に発現し,IRF8.8によって調節されます.
- L-Mycの発現は,c-Mycの発現が減少するにつれて,一般的なDCの祖先で開始されます.
- Mycl1欠乏したマウスは,移動性CD103 (((+)) の従来のDCを含む,特異的なDCサブセットの減少を示しています.
- DCにおけるL-Mycの喪失は,Listeria monocytogenesおよび膀性口炎ウイルス感染中に,体内のT細胞のプライミングを著しく阻害する.
結論:
- L-Mycは,特定の dendritic 細胞のサブセットの発達と機能において,重要かつ非冗長な役割を果たします.
- DCにおけるL-Mycの選択的発現と調節は,免疫反応における特異的な機能を示唆している.
- L-Mycは,炎症中のDCに不可欠なMyc転写活性を提供し,最適のT細胞プライミングを促進する可能性があります.
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