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mTORは,肺内のAPCの代謝適応を調節し,アレルギー性炎症の結果を制御する.

  • 0Emory Vaccine Center, Emory University, 954 Gatewood Road NE, Atlanta, GA 30329, USA.
Clinical Neuroscience (new York, N.y.) +

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2017年8月12日

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2017年8月12日

PubMedで要約を見る

まとめ

この要約は機械生成です。

ラパミシン (mTOR) のメカニズム標的は,特定の組織における免疫細胞の代謝を制御する. この代謝適応はアレルギー性炎症に影響を与え,免疫反応をTヘルパー2 (T<sub>H</sub>2) からTヘルパー17 (T<sub>H</sub>17) タイプにシフトさせます.

科学分野

  • 免疫学
  • 細胞の代謝
  • 炎症に関する研究

背景

  • 抗原を提示する細胞 (APC) は様々な組織に存在するが,その局所的調節は不明である.
  • 組織特異的な免疫細胞の恒常性を理解することは,免疫応答の調節に不可欠です.

研究 の 目的

  • 組織に制限されたAPCホメオスタシスと代謝適応におけるラパミシン (mTOR) の機械的標的の役割を調査する.
  • APCにおけるmTOR依存の代謝変化がアレルギー性炎症にどのように影響するかを決定する.

主な方法

  • 異なる解剖学的な場所でのAPCを研究するために炎症のマウスモデルを使用しました.
  • dendritic cell (DC) と alveolar macrophageの代謝と機能に対するmTOR欠乏の影響を分析した.
  • 変化したDC代謝に対する反応として,アレルギー性炎症の偏向の変化 (T<sub>H</sub>2対T<sub>H</sub>17) を評価した.

主要な成果

  • mTORはリンパ性組織におけるDCホメオスタシスには欠かせないが,肺CD103+DCとアルベオラマクロファージには不可欠である.
  • mTOR欠乏症の肺CD11b+DCは,数値的な変化ではなく,代謝の再プログラムを示した.
  • この再プログラムにより,T<sub>H</sub>2からT<sub>H</sub>17へのアレルギー性炎症は,IL-23の産生と脂肪酸の酸化の増加によって引き起こされた.

結論

  • mTORは組織特異のAPCにおける重要な代謝適応を媒介する.
  • これらの代謝適応は,アレルギー性炎症反応の種類と重さに直接影響を及ぼします.
  • mTORをターゲットにすることで アレルギー性炎症を調節する 戦略を提供できます

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