efferocytotic engulfment (Galectin Therapeutics)
Structured Review
![The role of efferocytosis by immune cells in infections. Efferocytosis participates in host defense against invading microbes. However, certain pathogens can escape efferocytosis and accelerate their spread. Efferocytosis is accomplished by professional and unprofessional phagocytes. Remarkably, macrophages and dendritic cells are professional phagocytes that are the most commonly studied of the efferocytes. (A) Ingestion of infected apoptotic cells by macrophages limits secondary necrosis of these cells and bacteria release, thereby improving bacteria clearance. In some cases, certain bacteria can trigger pyroptosis in infected cells. <t>Efferocytotic</t> receptors (i.e., scavenger receptor, complement receptor) are able to recognize pore-induced intracellular traps (PITs) and pytoptotic neutrophil containing bacteria. Subsequently, the process results in bacteria killing via infusion of phagosome to lysosome. However, some pathogens [e.g., methicillin-resistant Staphylococcus aureus (MRSA)] escape efferocytosis through “tolerate me” signal CD47 and signal regulatory protein α (SIRPα) on the infected cells. (B) Recognition and internalization of some viruses [such as herpes simplex virus type 1 (HSV-1)]-infected cells by dendritic cells interact with RAN-binding protein 9 (RANBP9), low-density lipoprotein receptor-related protein 1 (LRP1), and a protein complex comprising AXL. The cross presentation of viral antigen by dendritic cells on MHC class I molecules induces differentiation of CD8 + T cells against viruses. Similarly, dendritic cells swallow infected cells and thereby promote expansion of anti-bacteria effector T cells. In the infected cells, pathogen-associated molecular patterns (PAMPs) signal via Toll-like receptors (TLRs) and stimulate production of transforming growth factor-beta (TGF-β) and interleukin (IL)-6, thereby expanding the population of CD4 + T cells to T helper (Th)17 cells but inhibiting generation of regulatory T (Treg) cells.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_3510/pmc08913510/pmc08913510__fcell-10-839248-g002.jpg)
Efferocytotic Engulfment, supplied by Galectin Therapeutics, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 86 stars, based on 1 article reviews
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1) Product Images from "Efferocytosis and Its Role in Inflammatory Disorders"
Article Title: Efferocytosis and Its Role in Inflammatory Disorders
Journal: Frontiers in Cell and Developmental Biology
doi: 10.3389/fcell.2022.839248
![... certain bacteria can trigger pyroptosis in infected cells. Efferocytotic receptors (i.e., scavenger receptor, complement receptor) are able ... The role of efferocytosis by immune cells in infections. Efferocytosis participates in host defense against invading microbes. However, certain pathogens can escape efferocytosis and accelerate their spread. Efferocytosis is accomplished by professional and unprofessional phagocytes. Remarkably, macrophages and dendritic cells are professional phagocytes that are the most commonly studied of the efferocytes. (A) Ingestion of infected apoptotic cells by macrophages limits secondary necrosis of these cells and bacteria release, thereby improving bacteria clearance. In some cases, certain bacteria can trigger pyroptosis in infected cells. Efferocytotic receptors (i.e., scavenger receptor, complement receptor) are able to recognize pore-induced intracellular traps (PITs) and pytoptotic neutrophil containing bacteria. Subsequently, the process results in bacteria killing via infusion of phagosome to lysosome. However, some pathogens [e.g., methicillin-resistant Staphylococcus aureus (MRSA)] escape efferocytosis through “tolerate me” signal CD47 and signal regulatory protein α (SIRPα) on the infected cells. (B) Recognition and internalization of some viruses [such as herpes simplex virus type 1 (HSV-1)]-infected cells by dendritic cells interact with RAN-binding protein 9 (RANBP9), low-density lipoprotein receptor-related protein 1 (LRP1), and a protein complex comprising AXL. The cross presentation of viral antigen by dendritic cells on MHC class I molecules induces differentiation of CD8 + T cells against viruses. Similarly, dendritic cells swallow infected cells and thereby promote expansion of anti-bacteria effector T cells. In the infected cells, pathogen-associated molecular patterns (PAMPs) signal via Toll-like receptors (TLRs) and stimulate production of transforming growth factor-beta (TGF-β) and interleukin (IL)-6, thereby expanding the population of CD4 + T cells to T helper (Th)17 cells but inhibiting generation of regulatory T (Treg) cells.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_3510/pmc08913510/pmc08913510__fcell-10-839248-g002.jpg)
Figure Legend Snippet: The role of efferocytosis by immune cells in infections. Efferocytosis participates in host defense against invading microbes. However, certain pathogens can escape efferocytosis and accelerate their spread. Efferocytosis is accomplished by professional and unprofessional phagocytes. Remarkably, macrophages and dendritic cells are professional phagocytes that are the most commonly studied of the efferocytes. (A) Ingestion of infected apoptotic cells by macrophages limits secondary necrosis of these cells and bacteria release, thereby improving bacteria clearance. In some cases, certain bacteria can trigger pyroptosis in infected cells. Efferocytotic receptors (i.e., scavenger receptor, complement receptor) are able to recognize pore-induced intracellular traps (PITs) and pytoptotic neutrophil containing bacteria. Subsequently, the process results in bacteria killing via infusion of phagosome to lysosome. However, some pathogens [e.g., methicillin-resistant Staphylococcus aureus (MRSA)] escape efferocytosis through “tolerate me” signal CD47 and signal regulatory protein α (SIRPα) on the infected cells. (B) Recognition and internalization of some viruses [such as herpes simplex virus type 1 (HSV-1)]-infected cells by dendritic cells interact with RAN-binding protein 9 (RANBP9), low-density lipoprotein receptor-related protein 1 (LRP1), and a protein complex comprising AXL. The cross presentation of viral antigen by dendritic cells on MHC class I molecules induces differentiation of CD8 + T cells against viruses. Similarly, dendritic cells swallow infected cells and thereby promote expansion of anti-bacteria effector T cells. In the infected cells, pathogen-associated molecular patterns (PAMPs) signal via Toll-like receptors (TLRs) and stimulate production of transforming growth factor-beta (TGF-β) and interleukin (IL)-6, thereby expanding the population of CD4 + T cells to T helper (Th)17 cells but inhibiting generation of regulatory T (Treg) cells.
Techniques Used: Infection, Binding Assay