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STING 感知 微生物の生命力 ストレス媒介による内プラズマ網膜のオートファギーを調整する
Julien Moretti1, Soumit Roy2, Dominique Bozec3
1The Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY 10021, USA; Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY 10021, USA.
Cell
|October 24, 2017
まとめ
生きたバクテリアは,細胞の生存と免疫のために,内プラズマ網膜のストレスと自己死を引き起こす,サイクルディアデノシンモノフォスファート (Vita-PAMP) を介して危険を信号します.
科学分野:
- 免疫学
- 細胞生物学
- 微生物学
背景:
- 構成細胞自律免疫は,インターフェロン誘導反応に先立つ原始的な先天的防御である.
- ファゴサイトは,病原体関連分子パターン (PAMPs) によって誘発されるインターフェロン誘導反応を利用する.
- 感染中に構成細胞自律反応を誘発するシグナルについては,以前は知られていなかった.
研究 の 目的:
- 感染中に構成細胞自律免疫を誘発する信号を特定する.
- 微生物の生命力信号が先天的な免疫反応を活性化するメカニズムを解明する.
- 細胞のストレス反応が宿主の防御と生存にどのように貢献するか理解する.
主な方法:
- 先天的な免疫の活性化における微生物の生命力信号 (vita- PAMPs) の役割を調査した.
- 生きたグラム陽性細菌から採取したサイクリック・ディ・アデノシン・モノフォスファートは,特定のVita-PAMPとして利用した.
- インターフェロン遺伝子の刺激 (STING) と内プラズマ網膜 (ER) ストレスへの関与を調べた.
- ERストレスに対する反応としてラパミシン (mTOR) の非活性化と自己死性のメカニズム的標的の役割を評価した.
- ER-phagyのプロセスとSTINGの局所化とインターフェロン反応への影響を分析した.
主要な成果:
- 生のグラム陽性細菌におけるサイクルディアデノシンモノフォスファートが,PAMPの生命体として特定された.
- このVita-PAMPがSTINGを誘発し 細胞内膜のストレスを引き起こすことが示されました
- ERのストレスはmTORを無効化し,ERの収束とストレスの解消のためにオートファギーを動員します.
- ビタ-PAMP誘発の ER-phagyは ERのストレスを解消し,ファゴシートの死を防ぐことが判明しました.
- ER-phagyが インターフェロン反応を誘導し ER-レジデントのSTINGを オートファゴソームに 移動させることがわかりました
結論:
- ストレス媒介のERファギーは,特定のVita-PAMPのSTING依存感知によって活性化された細胞自律の免疫反応である.
- 生まれながらの受容体は,多層のホメオスタティックメカニズムを活性化し,感染後の免疫と生存を促進します.
- この経路は 細胞のストレス,オートファジー,先天的な免疫活性化との 重要な関係を強調しています
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