We are analyzing https://link.springer.com/article/10.1007/s00281-018-0698-5.

Title:
Efferocytosis in the tumor microenvironment | Seminars in Immunopathology
Description:
Within the course of a single minute, millions of cells in the human body will undergo programmed cell death in response to physiological or pathological cues. The diminished energetic capacity of an apoptotic cell renders the cell incapable of sustaining plasma membrane integrity. Under these circumstances, intracellular contents that might leak into the surrounding tissue microenvironment, a process referred to as secondary necrosis, could induce inflammation and tissue damage. Remarkably, in most cases of physiologically rendered apoptotic cell death, inflammation is avoided because a mechanism to swiftly remove apoptotic cells from the tissue prior to their secondary necrosis becomes activated. This mechanism, referred to as efferocytosis, uses phagocytes to precisely identify and engulf neighboring apoptotic cells. In doing so, efferocytosis mantains tissue homeostasis that would otherwise be disrupted by normal cellular turnover and exacerbated further when the burden of apoptotic cells becomes elevated due to disease or insult. Efferocytosis also supports the resolution of inflammation, restoring tissue homesostasis. The importance of efferocytosis in health and disease underlies the increasing research efforts to understand the mechanisms by which efferocytosis occurs, and how a failure in the efferocytic machinery contributes to diseases, or conversely, how cancers effectively use the existing efferocytic machinery to generate a tumor-tolerant, immunosuppressive tumor microenvironment. We discuss herein the molecular mechanisms of efferocytosis, how the process of efferocytosis might support a tumor ‘wound healing’ phenotype, and efforts to target efferocytosis as an adjunct to existing tumor treatments.
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Keywords {🔍}

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Topics {✒️}

c1q–calreticulin–phosphatidylserine interactions yield antigen-dependent anti-tumor immunity anti-inflammatory cytokine-encoding genes efferocytosis-induced anti-inflammatory cytokines full size image article download pdf wild-type bone marrow post-lactational involution removes peroxisome proliferator-activated receptor post-partum mammary gland p63/p73 target gene monoclonal anti-phosphatidylserine antibody anti-inflammatory phenotype generated apoptotic human t-cells specific anti-migratory effects apoptotic jurkat cells—existence triple-negative breast cancers highly pro-inflammatory event phosphatidylserine-dependent homeostatic response small-cell lung cancer inflammation-resolving cytokines produced membrane-encapsulated dying cell ligand-activated lxrα/pparγ activate wound-healing signaling events efferocytosis-induced tumor progression elmo/dock180/rac module alphavbeta5 integrin-mediated phagocytosis epithelial cell-directed efferocytosis resultant anti-inflammatory response integrin-activating protein expressed produce anti-inflammatory cytokines fully immune-competent mice autophagy-related proteins ulk1 mertk-gas6 bridging combinations unconventional rac-gef activity pro-tumorogenic effect primarily transforming growth factor postpartum mammary gland mertk small-molecule inhibitor mertk-mediated efferocytosis promotes mitochondrial fission influences pro-tolerogenic tumor microenvironment tumor necrosis factor mertk-related rtks axl mitochondrial fission promotes inflammation-induced tissue damage receptor tyrosine kinase pro-inflammatory damps released privacy choices/manage cookies ptdser-binding molecules expressed

Schema {🗺️}

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         headline:Efferocytosis in the tumor microenvironment
         description:Within the course of a single minute, millions of cells in the human body will undergo programmed cell death in response to physiological or pathological cues. The diminished energetic capacity of an apoptotic cell renders the cell incapable of sustaining plasma membrane integrity. Under these circumstances, intracellular contents that might leak into the surrounding tissue microenvironment, a process referred to as secondary necrosis, could induce inflammation and tissue damage. Remarkably, in most cases of physiologically rendered apoptotic cell death, inflammation is avoided because a mechanism to swiftly remove apoptotic cells from the tissue prior to their secondary necrosis becomes activated. This mechanism, referred to as efferocytosis, uses phagocytes to precisely identify and engulf neighboring apoptotic cells. In doing so, efferocytosis mantains tissue homeostasis that would otherwise be disrupted by normal cellular turnover and exacerbated further when the burden of apoptotic cells becomes elevated due to disease or insult. Efferocytosis also supports the resolution of inflammation, restoring tissue homesostasis. The importance of efferocytosis in health and disease underlies the increasing research efforts to understand the mechanisms by which efferocytosis occurs, and how a failure in the efferocytic machinery contributes to diseases, or conversely, how cancers effectively use the existing efferocytic machinery to generate a tumor-tolerant, immunosuppressive tumor microenvironment. We discuss herein the molecular mechanisms of efferocytosis, how the process of efferocytosis might support a tumor ‘wound healing’ phenotype, and efforts to target efferocytosis as an adjunct to existing tumor treatments.
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      headline:Efferocytosis in the tumor microenvironment
      description:Within the course of a single minute, millions of cells in the human body will undergo programmed cell death in response to physiological or pathological cues. The diminished energetic capacity of an apoptotic cell renders the cell incapable of sustaining plasma membrane integrity. Under these circumstances, intracellular contents that might leak into the surrounding tissue microenvironment, a process referred to as secondary necrosis, could induce inflammation and tissue damage. Remarkably, in most cases of physiologically rendered apoptotic cell death, inflammation is avoided because a mechanism to swiftly remove apoptotic cells from the tissue prior to their secondary necrosis becomes activated. This mechanism, referred to as efferocytosis, uses phagocytes to precisely identify and engulf neighboring apoptotic cells. In doing so, efferocytosis mantains tissue homeostasis that would otherwise be disrupted by normal cellular turnover and exacerbated further when the burden of apoptotic cells becomes elevated due to disease or insult. Efferocytosis also supports the resolution of inflammation, restoring tissue homesostasis. The importance of efferocytosis in health and disease underlies the increasing research efforts to understand the mechanisms by which efferocytosis occurs, and how a failure in the efferocytic machinery contributes to diseases, or conversely, how cancers effectively use the existing efferocytic machinery to generate a tumor-tolerant, immunosuppressive tumor microenvironment. We discuss herein the molecular mechanisms of efferocytosis, how the process of efferocytosis might support a tumor ‘wound healing’ phenotype, and efforts to target efferocytosis as an adjunct to existing tumor treatments.
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         Apoptotic cell death
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         Phosphatidyl serine, macrophage
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         Internal Medicine
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               type:PostalAddress
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      name:Program in Cancer Biology, Vanderbilt University School of Medicine, Nashville, USA
      name:Vanderbilt Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, USA
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