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NRROSは,宿主防御と自己免疫の間に反応性酸素種を否定的に調節する

Rajkumar Noubade¹, Kit Wong², Naruhisa Ota²

¹1] Department of Immunology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA [2] Flexus Biosciences, 75 Shoreway Road, Suite D, San Carlos, California 94070, USA (R.N.); American Society for Biochemistry and Molecular Biology, 11200 Rockville Pike, Suite 302, Rockville, Maryland 20852, USA (P.A.V.).

|April 18, 2014

まとめ

新しく発見されたタンパク質,ROS (NRROS) のネガティブレギュレータは,ファゴサイトにおける反応性酸素種 (ROS) の生成を制御する. NRROS欠乏症は病原体の防御を強化するが,自己免疫損傷のリスクがあり,免疫応答の重要な調節体を明らかにする.

科学分野:

免疫学免疫学とは
細胞生物学細胞生物学
バイオケミストリーバイオケミストリー

背景:

胞由来反応性酸素種 (ROS) は,病原体に対する宿主防御に不可欠です.
調節不能のROS産生は,慢性粒状小胞性疾患と炎症性組織損傷に寄与する.
ROSの厳格な調節は,免疫のバランスと自己免疫の予防に不可欠です.

研究の目的:

ファゴサイトにおけるROS生成の新たなレギュレータを特定し,特徴づけること.
NRROSがROS生成を制御するメカニズムを解明する.
宿主防御および炎症性疾患におけるNRROSの生理学的役割を調査する.

主な方法:

ROS (NRROS) のネガティブレギュレータである新しいタンパク質を特定し,特徴づけました.
NRROS欠乏性ファゴサイトとノックアウトマウスモデルを使用した.
バイオケミカルアッセイと細胞局所化研究を用いてNRROSの機能を調査した.
エンドプラズマ網膜におけるNRROSとNOX2サブユニットの相互作用を調べた.

主要な成果:

NRROSは,炎症時のファゴサイトによるROS生成を制限する.
NRROS欠乏性ファゴサイトは,ROSの産生が増加し,細菌滅菌活動が強化される.
NRROSが欠けているマウスは,酸化的ダメージによる自己免疫疾患に対する感受性の増加を示しています.
NRROSはNOX2と相互作用し,ERに関連する分解を介してその分解を促進します.

結論:

NRROSは,ファゴシトのROS生成の新種の負の調節剤である.
NRROSは宿主の防御を均衡させ,自己免疫組織の損傷を防ぐ上で重要な役割を果たします.
NRROSを標的にすることは,感染症および炎症性疾患の治療戦略を提供することができる.

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