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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
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新しい転写因子であるT-betは,Th1系統へのコミットメントを指示する
S J Szabo1, S T Kim, G L Costa
1Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA.
Cell
|April 13, 2000
まとめ
Th1特異の転写因子であるT-betは,Tヘルパー細胞の分化を促進する. IFNgamma遺伝子を活性化し,Th2サイトカインを抑制し,Th1系統の発達を開始します.
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.
- 細胞生物学 細胞生物学
背景:
- ネイブTヘルパー細胞は,別々のTh1およびTh2サブセットに微分化します.
- これらのサブセットは,適応免疫に不可欠なユニークな機能とサイトカインプロファイルを持っています.
研究 の 目的:
- Th1細胞の分化に関与する転写因子であるT-betを特定し,特徴づけること.
- 主要なTh1およびTh2サイトカインの発現を制御するT-betの役割を明らかにする.
主な方法:
- T-ベットの転写因子の分離と特徴付け.
- Th1,Th2,NK細胞におけるT-ベットの発現の分析.
- 主要T細胞におけるT-ベットの子宮外発現に関する研究.
- 系統のリダイレクトを評価するためにレトロウイルス遺伝子トランスデュークション.
主要な成果:
- T-ベットの発現は,Th1およびNK細胞におけるインターフェロン・ガンマ (IFNgamma) 発現と直接相関する.
- エクトピックTベットの発現はIFNgamma遺伝子を活性化し,IFNgammaの産生を誘導する.
- Tベットのトランスデュークションは,偏ったTh2/Tc2細胞をTh1/Tc1フェノタイプにリダイレクトし,IL-4とIL-5を抑制しながらIFNgammaを誘導します.
結論:
- T-betは,Th1系統の発達を開始する重要な転写因子です.
- T-betは,Th1特異遺伝子を活性化し,Th2特異遺伝子を抑制することによってTh1の分化をオーケストラします.
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