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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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Apoptosis01:30

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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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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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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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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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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Author Spotlight: THP-1 Macrophage Response to LPS/ATP &#8212; Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum
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Plasma membrane changes during programmed cell deaths.

Yingying Zhang1, Xin Chen1, Cyril Gueydan2

  • 1State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361005, China.

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|October 28, 2017
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Summary
This summary is machine-generated.

Cell death pathways like apoptosis, necroptosis, and pyroptosis involve distinct plasma membrane changes. Understanding these membrane events is key to how dying cells trigger immune responses.

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Area of Science:

  • Cell Biology
  • Immunology

Background:

  • Apoptosis (programmed cell death) was traditionally viewed as non-inflammatory, while necrosis was inflammatory.
  • Necroptosis and pyroptosis are programmed necrosis forms with distinct plasma membrane pore mechanisms (MLKL channels vs. gasdermin D pores).

Purpose of the Study:

  • To review recent advances in apoptosis, necroptosis, and pyroptosis.
  • To emphasize plasma membrane changes during cell death.
  • To explore the implications of these changes in cell death-elicited immunogenicity.

Main Methods:

  • Literature review of recent studies on programmed cell death.
  • Analysis of mechanisms underlying plasma membrane pore formation.
  • Discussion of the role of intracellular contents released during cell death.

Main Results:

  • Plasma membrane rupture in necroptosis is MLKL-mediated, while pyroptosis involves gasdermin D pores.
  • Secondary necrosis can be programmed via plasma membrane pores, similar to pyroptosis.
  • Distinct cell death programs cause unique plasma membrane alterations.

Conclusions:

  • Plasma membrane integrity and breakdown mechanisms significantly influence cell fate and immunogenicity.
  • The nature of released intracellular contents is critical for immune responses to dying cells.
  • Understanding plasma membrane dynamics in cell death is crucial for immunogenicity research.