The Dynamics of Apoptotic Cell Clearance

Elliott, Michael R.; Ravichandran, Kodi S.

doi:10.1016/j.devcel.2016.06.029

Cited by 262 publications

(254 citation statements)

References 175 publications

(301 reference statements)

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“…These data suggest that the reduced platelets resulted from apoptosis-induced platelet However, injection of anti-platelet mixture antibody R300, which incurs platelet apoptosis (Supplemental Figure 12), induced more rapid platelet clearance in PKA +/-mice than in PKA +/+ mice ( Figure 4G), suggesting that the PKA +/-platelets are more prone to apoptosis. It has been well established that apoptotic cells are rapidly cleared by phagocytes in vivo (31,32). We found that the number of circulatory platelets was markedly reduced in the destruction.…”

mentioning

confidence: 56%

Protein kinase A determines platelet life span and survival by regulating apoptosis

Zhao

et al. 2017

Journal of Clinical Investigation

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mentioning

confidence: 56%

Protein kinase A determines platelet life span and survival by regulating apoptosis

Zhao

et al. 2017

Journal of Clinical Investigation

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“…Key find-me signals identified to date include triphosphate nucleotides (ATP, UTP) (30, 31), the chemokine CX3CL1 (32), and the signaling lipids lysophosphatidylcholine (lysoPC) and sphingosine-1-phosphate (S1P) (33–35). While all of these factors can stimulate macrophage migration to apoptotic cells, the relevance of individual find-me signals in efferocytosis depends on many factors, including phagocyte and apoptotic cell type as well as the apoptotic stimuli and the stage of apoptosis being studied (reviewed in (36)). As discussed below, some of these find-me signals also function as key modulators of macrophage inflammatory responses.…”

Section: Introductionmentioning

confidence: 99%

Efferocytosis Signaling in the Regulation of Macrophage Inflammatory Responses

Elliott

Koster

Murphy

2017

The Journal of Immunology

335

274

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Since the pioneering work of Elie Metchnikoff and the discovery of cellular immunity, the phagocytic clearance of cellular debris has been considered an integral component of resolving inflammation and restoring function of damaged and infected tissues. We now know that the phagocytic clearance of dying cells (efferocytosis), particularly by macrophages and other immune phagocytes, has profound consequences on innate and adaptive immune responses in inflamed tissues. These immunomodulatory effects result from an array of molecular signaling events between macrophages, dying cells and other tissue-resident cells. In recent years, many of these molecular pathways have been identified and studied in the context of tissue inflammation, helping us better understand the relationship between efferocytosis and inflammation. We review specific types of efferocytosis-related signals that can impact macrophage immune responses and discuss their relevance to inflammation-related diseases.

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“…Removal of dead or dying cells by efferocytosis is critical for maintaining homeostasis and preventing inflammation and autoimmune reactions (Elliott and Ravichandran, 2016). Because infection by certain viruses induces massive cell death, efferocytosis plays an important role in maintaining host homeostasis during viral infection (Jorgensen et al, 2017; Nainu et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Protein S and Gas6 induce efferocytosis of HIV-1-infected cells

et al. 2018

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Efferocytosis, the phagocytic clearance of apoptotic cells, can provide host protection against certain types of viruses by mediating phagocytic clearance of infected cells undergoing apoptosis. It is known that HIV-1 induces apoptosis and HIV-1-infected cells are efferocytosed by macrophages, although its molecular mechanisms are unknown. To elucidate the roles that efferocytosis of HIV-1-infected cells play in clearance of infected cells, we sought to identify molecules that mediate these processes. We found that protein S, present in human serum, and its homologue, Gas6, can mediate phagocytosis of HIV-1-infected cells by bridging receptor tyrosine kinase Mer, expressed on macrophages, to phosphatidylserine exposed on infected cells. Efferocytosis of live infected cells was less efficient than dead infected cells; however, a significant fraction of live infected cells were phagocytosed over 12 h. Our results suggest that efferocytosis not only removes dead cells, but may also contribute to macrophage removal of live virus producing cells.

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The Dynamics of Apoptotic Cell Clearance

Cited by 262 publications

References 175 publications

Protein kinase A determines platelet life span and survival by regulating apoptosis

Protein kinase A determines platelet life span and survival by regulating apoptosis

Efferocytosis Signaling in the Regulation of Macrophage Inflammatory Responses

Protein S and Gas6 induce efferocytosis of HIV-1-infected cells

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