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Related Concept Videos

Necrosis01:16

Necrosis

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Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
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The innate immune response is an immediate and non-specific response against pathogens, acting swiftly to prevent the spread of infections. The primary cells involved in this response are phagocytes and natural killer (NK) cells.
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Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
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Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
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Cytotoxic T Cells-mediated Immune Response01:27

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Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
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Updated: Jul 19, 2025

Evaluation of Caspase Activation to Assess Innate Immune Cell Death
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Programmed Necrosis in Host Defense.

Edward S Mocarski1,2

  • 1Robert W. Woodruff Professor Emeritus, Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, 30322, USA. mocarski@stanford.edu.

Current Topics in Microbiology and Immunology
|August 10, 2023
PubMed
Summary

Mammalian cells use cell death pathways like apoptosis and necroptosis to fight viral infections. Viruses counter these defenses, but Z-nucleic acid sensor ZBP1 plays a key role in recognizing viral threats.

Keywords:
ApoptosisHerpesvirusNecroptosisPoxvirusProgramed cell deathZ-nucleic acid binding protein

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Area of Science:

  • Immunology
  • Cell Biology
  • Virology

Background:

  • Host immune systems rely on cellular defense mechanisms to combat infectious diseases.
  • Pathogens evolve strategies to evade or suppress host immune responses, including cell death pathways.
  • Cell autonomous signaling pathways initiate inflammatory responses, deploy restriction factors, and induce cell death upon pathogen invasion.

Purpose of the Study:

  • To explore the intricate interplay between viruses and host cell death machinery.
  • To highlight the role of programmed cell death pathways in controlling viral infections.
  • To emphasize the significance of Z-nucleic acid sensor ZBP1 in detecting viral pathogens.

Main Methods:

  • Review of established and emerging literature on host-pathogen interactions and cell death.
  • Analysis of signaling pathways involved in apoptosis and necroptosis.
  • Investigation of viral strategies to inhibit host cell death mechanisms.

Main Results:

  • Diverse cell death pathways, including apoptosis and necroptosis, are crucial for early control of viral infections.
  • Activation of death receptors (DRs), toll-like receptors (TLRs), or Z-nucleic acid binding protein 1 (ZBP1) can trigger apoptosis or necroptosis.
  • Viruses, such as herpesviruses and poxviruses, encode suppressors to block these host cell death pathways.

Conclusions:

  • Z-nucleic acid sensor ZBP1 is vital for the cell autonomous recognition of DNA and RNA virus infections.
  • Understanding the 'detente' between viruses and host cell death machinery is key to controlling viral spread.
  • Targeting viral suppression of cell death pathways offers potential therapeutic strategies against viral diseases.