Article

Beginnings of a Good Apoptotic Meal: The Find-Me and Eat-Me Signaling Pathways

Department of Microbiology, Immunology, and Cancer Biology, Center for Cell Clearance, University of Virginia, Charlottesville, VA 22908, USA.
Immunity (Impact Factor: 21.56). 10/2011; 35(4):445-55. DOI: 10.1016/j.immuni.2011.09.004
Source: PubMed

ABSTRACT

Prompt and efficient clearance of apoptotic cells is necessary to prevent secondary necrosis of dying cells and to avoid immune responses to autoantigens. Recent studies have shed light on how apoptotic cells through soluble "find-me" signals advertise their presence to phagocytes at the earliest stages of cell death. Phagocytes sense the find-me signal gradient, and in turn the presence of dying cells, and migrate to their vicinity. The apoptotic cells also expose specific "eat-me" signals on their surface that are recognized by phagocytes through specific engulfment receptors. This review covers the recent progress in the areas of find-me and eat-me signals and how these relate to prompt and immunologically silent clearance of apoptotic cells.

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Available from: Kodi Ravichandran, May 26, 2014
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    • "After initial steps of apoptosis, neutrophils lose their functional properties, such as the ability to move by chemotaxis , generate a respiratory burst, or degranulate[95]. Furthermore, they exhibit alterations on their intracellular pathways and cell surface molecules while some externalized molecules, such as phosphatidylserines (PS), facilitate the recognition and removal of apoptotic neutrophils by macro- phages[92,96]. Recent studies have reported that AnxA1 from apoptotic cells is involved in their phagocytic clearance. "
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    • "A summary of characteristics of these PVEERs is shown in Table 1. The key property that these proteins or complexes utilize to enhance virus entry is their ability to bind PtdSer and a native function of all of these receptors is to bind and clear apoptotic bodies (Ravichandran, 2011). Mutation of residues involved in PtdSer binding or complex formation results in inhibition of PVEER function (Morizono et al., 2011; Meertens et al., 2012; Moller-Tank et al., 2013; Morizono and Chen, 2014). "
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