炎症におけるプログラム性死滅:効果分子識別に向けて

David Wallach¹, Tae-Bong Kang², Christopher P Dillon³

¹Department of Biomolecular Sciences, The Weizmann Institute of Science, 76100 Rehovot, Israel. d.wallach@weizmann.ac.il douglas.green@stjude.org.

Science (New York, N.Y.)

|April 2, 2016

まとめ

プログラムされた細胞死にはアポトーシスやプログラムされた死滅のような異なる経路が含まれます最近のMLKLやガスダーミン-Dのような分子の発見は炎症を理解する上で鍵となるものです

科学分野:

細胞生物学
免疫学
分子生物学

背景:

プログラムされた細胞死は歴史的に統一されたプロセスと見なされていました
アポトーシスとプログラムされた死滅を含む細胞死の異なる経路が新しく明らかになっています
プログラムされた死滅は免疫刺激成分を放出します破壊性の少ないアポトーシスとは違います

研究の目的:

プログラム細胞死亡のメカニズムを区別する
プログラムされた死滅を媒介する分子を特定する
炎症における死細胞の役割のよりよい評価を促すため

主な方法:

プログラムされた細胞死における最近の分子発見のレビュー
末期の死路に関わるタンパク質の分析
アポプトーシス,ネクロプトーシス,およびパイロプトーシスにおける分子要素の比較.

主要な成果:

アポトーシス以外のプログラム細胞死経路の特定
ネクロプトーシス (MLKL) とパイロプトーシス (ガスダーミン-D) の主要な媒介体の発見
早期の死滅媒介体 (RIPK1,RIPK3,カスパース-1) にプレイオトロプ的機能があることを認識する.

結論:

異なる分子の経路がプログラムされた細胞死の異なる形態を制御します
MLKLやガスダーミンDのような遅発性タンパク質は,特定の死滅の実行に不可欠です.
これらの発見は,炎症プロセスにおける死滅細胞のインビボの役割を調査するために不可欠なツールを提供します.

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