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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 extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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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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Related Experiment Video

Updated: Dec 16, 2025

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Flipping the Switch from Inflammation to Cell Death.

Hayley I Muendlein1, Alexander Poltorak2

  • 1Graduate Program in Genetics, Tufts Graduate School of Biomedical Sciences, Boston, MA 02111, USA.

Trends in Immunology
|July 6, 2020
PubMed
Summary
This summary is machine-generated.

Cellular FLICE-like inhibitory protein (cFLIP) regulates pyroptosis, a form of programmed cell death. cFLIP deficiency offers a model to investigate caspase-8 (CASP8)-mediated cell death and inflammation.

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Evaluation of Caspase Activation to Assess Innate Immune Cell Death
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Evaluation of Caspase Activation to Assess Innate Immune Cell Death

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Area of Science:

  • Cellular biology
  • Immunology
  • Molecular mechanisms of cell death

Background:

  • Caspase-8 (CASP8)-mediated gasdermin D (GSDMD) cleavage is a known driver of pyroptotic cell death.
  • Pyroptosis is a highly inflammatory form of programmed cell death.
  • The precise regulatory mechanisms of CASP8 activation in cell death pathways require further elucidation.

Purpose of the Study:

  • To investigate the role of the long isoform of cellular FLICE-like inhibitory protein (cFLIPL) in pyroptosis.
  • To establish a cFLIP-deficient model for studying CASP8-mediated cell death and inflammatory signaling.

Main Methods:

  • Utilizing a cFLIP-deficient cellular model.
  • Analyzing CASP8 activity and GSDMD cleavage.
  • Assessing pyroptotic cell death and inflammatory cytokine release.

Main Results:

  • Demonstrated that cFLIPL, an inactive CASP8 homolog, plays a regulatory role in pyroptosis.
  • Showcased the utility of cFLIP-deficient cells for dissecting CASP8-mediated inflammatory signaling.
  • Highlighted the complex interplay between cFLIP and CASP8 in controlling cell death outcomes.

Conclusions:

  • cFLIP is a key regulator of CASP8-mediated pyroptosis.
  • cFLIP deficiency provides a valuable tool for understanding the initiation and execution of pyroptosis.
  • Further research into cFLIP's function can reveal novel therapeutic targets for inflammatory diseases.