Abstract
The apoptotic death of cells is accompanied by the exposure of “eat-me” signals that serve to prevent necrotic degradation of apoptotic cells, and thereby prevent inflammation, promote resolution of immune responses, and stimulate tissue repair. These “eat-me” signals include the exposure of phosphatidylserine (PS) on the outer plasma membrane during the early stages of apoptosis as well as on the surface of apoptotic bodies, plasma membrane vesicles that are shed during the later stages of cell death. In our recent publication (PLoS Biol. 15(6):e2002711), we describe similar ‘eat-me’ and ‘find-me’ signals present during necroptosis, challenging some of our common assumptions about regulated forms of lytic death.
Highlights
Several new types of regulated cell death have emerged from analysis of necrotic forms of cell death; one example is necroptosis, a RIPK3-MLKL-dependent and caspaseindependent form of cell death
These “eat-me” signals include the exposure of phosphatidylserine (PS) on the outer plasma membrane during the early stages of apoptosis as well as on the surface of apoptotic bodies, plasma membrane vesicles that are shed during the later stages of cell death
We showed that PS is externalized to the outer plasma membrane of necroptotic cells prior to the loss of plasma membrane integrity
Summary
Several new types of regulated cell death have emerged from analysis of necrotic forms of cell death; one example is necroptosis, a RIPK3-MLKL-dependent and caspaseindependent form of cell death. 1 Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel. * Corresponding Author: Motti Gerlic, Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel; E-mail: mgerlic@post.tau.ac.il
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