TH17細胞のコントロールは,小腸で起こります
Enric Esplugues1, Samuel Huber, Nicola Gagliani
1Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. enric.esplugues@yale.edu
Nature
|July 19, 2011
まとめ
自己免疫疾患に関与する炎症誘発性Tヘルパー17 (T(H) (17) 細胞は,小腸で制御されています. これらの細胞は除去されるか,制御性T (H) 17細胞に変換され,病原性を制限する.
科学分野:
- 免疫学 免疫学とは
- 細胞生物学 細胞生物学
背景:
- インターレウキン17を産生するTヘルパー細胞 (T(H) 17) は,CD4(+) T細胞の別々のサブセットである.
- T (H) 17細胞は,実験的自己免疫脳内炎 (EAE) のような自己免疫疾患の主要な原動力である.
- vivoでT(H) 17細胞を制御するメカニズムは,依然としてほとんど不明です.
研究 の 目的:
- 免疫系がプロ炎症性T (H) 17細胞をどのように,どこで制御するかを in vivoで調査する.
- T(H) 17細胞の病原性を制限するメカニズムを特定する.
主な方法:
- 耐性誘導,セプシス,インフルエンザAウイルス感染症 (H1N1) のモデルを使用した.
- CCR6/CCL20軸経由で研究されたT(H) 17細胞の移動.
- 小腸で評価されたT(H) 17細胞の除去とフェノタイプ変換.
主要な成果:
- 炎症を誘発するT (H) 17細胞は,小腸に移動し,小腸内で制御される.
- 小腸におけるCCL20ケモカイン発現は,T(H) 17細胞ホーミングを促進する.
- T(H) 17細胞は,腸の膜を通って排出されるか,または,免疫抑制性,免疫抑制性 (rT(H) 17) を獲得する.
結論:
- 小腸は,病原性T (H) 17細胞を制御する重要な部位として機能します.
- そのメカニズムには,自己免疫反応を緩和する,制御性T(H) 17細胞への除去と変換が含まれています.
- これらの発見は,免疫ホメオスタシスとT(H) 17細胞の調節における胃腸の役割を強調しています.
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