Bcl11bのデリレーションにより,T細胞を自然殺虫細胞に再プログラムする
Peng Li1, Shannon Burke, Juexuan Wang
1Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, UK.
Science (New York, N.Y.)
|June 12, 2010
まとめ
転写因子Bcl11bは,T細胞の発達に不可欠である. Bcl11bを削除すると,T細胞は腫瘍と戦う自然殺生細胞 (NK細胞) に変容し,新しい細胞療法アプローチを示唆します.
科学分野:
- 免疫学 免疫学とは
- 細胞生物学 細胞生物学
- 分子生物学は分子生物学である.
背景:
- T細胞は,胸腺で発達する適応性免疫にとって極めて重要です.
- ナチュラルキラー (NK) 細胞は,先天的な免疫の鍵であり,腫瘍の監視と病原体防御に関与します.
研究 の 目的:
- T細胞の発達における転写因子Bcl11bの役割を調査する.
- Bcl11bが欠けているT細胞の潜在的治療用途を調査する.
主な方法:
- Bcl11b発現の有無によるT細胞発達の分析.
- T細胞集団のBcl11bを削除するための遺伝子操作.
- 結果となる細胞の機能を評価するために,in vitroおよびin vivoアッセイを行います.
主要な成果:
- Bcl11bは,すべての段階においてT細胞系統の発達に不可欠である.
- T細胞におけるBcl11bの切除により,NK細胞の特性が誘発され,誘発されたTから自然殺人者 (ITNK) 細胞が生成された.
- ITNK細胞は,通常のNK細胞に似た形態と遺伝子発現を示し,腫瘍細胞の殺死と転移の予防を in vivo で実証した.
結論:
- Bcl11bは,T細胞のアイデンティティの重要なレギュレータです.
- ITNK細胞は,強力な抗腫瘍活性を持つ新しい細胞タイプを表しています.
- ITNKは,がんの免疫療法のための新しい細胞源として有望である.
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