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Published on: February 16, 2011
p38 MAPキナーゼ阻害による炭病致死因によるマクロファグアポプトシス
Jin Mo Park1, Florian R Greten, Zhi-Wei Li
1Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla, CA 92093-0636, USA.
Science (New York, N.Y.)
|August 31, 2002
まとめ
バシルス・アントラシス致死因 (LF) は,ミトゲン活性化タンパク質キナーゼ (MAPK) キナーゼを標的としてマクロファージのアポプトシスを誘導する. このメカニズムは宿主の先天的な免疫システムを麻痺させ,細菌の生存を助けます.
科学分野:
- 免疫学 免疫学とは
- 微生物学 微生物学とは
- 分子生物学は分子生物学である.
背景:
- バチルス・アントラシスは,マクロファージの死を誘発することによって,先天的な免疫を回避します.
- マクロファージは,先天的な免疫システムの重要な構成要素であり,病原体の検出と除去に不可欠です.
研究 の 目的:
- バチルス・アントラシスの致死因 (LF) がマクロファージのアポトーシスを誘発するメカニズムを解明する.
- LF誘発のアポトーシスが,先天性免疫の回避にどのように寄与するかを理解する.
主な方法:
- 活性化されたマクロファージに対するB. anthracis致死因の効果を調査した.
- LFによるミトゲン活性化タンパク質キナーゼ (MAPK) キナーゼ (MKKs) の分裂を分析した.
- マクロファージの生存におけるp38 MAPKと核因子kappaB (NF-kappaB) の役割を調べました.
主要な成果:
- B. anthracisの致死因は,活性化されたマクロファージで選択的にアポトーシスを誘発する.
- LFはMKKsのアミノ端末拡張を裂き,p38 MAPKの活性化を阻害する.
- p38 MAPKは,活性化マクロファージにおけるNF-kappaB媒介生存経路に不可欠である.
結論:
- バチルス・アントラシスは,p38 MAPKシグナリングモジュールを分解するために,致死因を使用します.
- このp38 MAPK経路の障害は宿主の先天的免疫を麻痺させ,細菌の生存を促進します.
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