Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK.
Trends Biochem Sci. 2012 Aug;37(8):325-32. doi: 10.1016/j.tibs.2012.05.002. Epub 2012 Jun 7.
Phagoptosis, also called primary phagocytosis, is a recently recognised form of cell death caused by phagocytosis of viable cells, resulting in their destruction. It is provoked by exposure of 'eat-me' signals and/or loss of 'don't-eat-me' signals by viable cells, causing their phagocytosis by phagocytes. Phagoptosis mediates turnover of erythrocytes, neutrophils and other cells, and thus is quantitatively one of the main forms of cell death in the body. It defends against pathogens and regulates inflammation and immunity. However, recent results indicate that inflamed microglia eat viable brain neurons in models of neurodegeneration, and cancer cells can evade phagocytosis by expressing a 'don't-eat-me' signal, suggesting that too much or too little phagoptosis can contribute to pathology. This review provides an overview of the molecular signals that regulate phagoptosis and the physiological and pathological circumstances in which it has been observed.
噬胞作用，也称为原发性吞噬作用，是一种最近被发现的细胞死亡形式，由吞噬活细胞引起，导致其被破坏。它是由活细胞暴露“吃我”信号和/或失去“别吃我”信号引起的，导致吞噬细胞吞噬它们。噬胞作用介导红细胞、中性粒细胞和其他细胞的更新，因此在数量上是体内主要的细胞死亡形式之一。它可以抵抗病原体并调节炎症和免疫。然而，最近的结果表明，在神经退行性变的模型中，炎症小胶质细胞吞噬活的大脑神经元，癌细胞可以通过表达“别吃我”信号来逃避吞噬作用，这表明噬胞作用过多或过少都可能导致病理学。这篇综述提供了调节噬胞作用的分子信号以及观察到噬胞作用的生理和病理情况的概述。
