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Related Concept Videos

The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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...
Apoptosis01:30

Apoptosis

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 reduction of the tissue.
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

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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Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
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Overview of Cell Death01:30

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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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Related Experiment Video

Updated: Jul 13, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Published on: December 27, 2016

Apoptosis-inducing factor regulates death in peripheral T cells.

Smita Srivastava1, Hridesh Banerjee, Ashutosh Chaudhry

  • 1National Institute of Immunology, New Delhi, India.

Journal of Immunology (Baltimore, Md. : 1950)
|July 10, 2007
PubMed
Summary

Apoptosis-inducing factor (Aif) plays dual roles in T cell death. Reduced Aif protects against neglect-induced death but increases susceptibility to activation-induced cell death, highlighting its complex regulation of T cell apoptosis.

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Apoptosis-inducing factor (Aif) is a mitochondrial protein involved in apoptosis, cellular respiration, and redox regulation.
  • The harlequin (Hq) mouse model exhibits reduced Aif expression due to a genetic modification.

Purpose of the Study:

  • To investigate the role of Aif in the regulation of peripheral T cell death pathways.
  • To determine if Aif influences susceptibility to neglect-induced death (NID) and activation-induced cell death (AICD).

Main Methods:

  • Analysis of T cell death in harlequin (Hq) mice compared to wild-type controls.
  • Assessment of Aif nuclear translocation and cytochrome c release during NID.
  • Evaluation of CD95L expression and susceptibility to hydrogen peroxide-induced apoptosis.
  • Investigation of superoxide scavenging effects on AICD.
  • siRNA-mediated knockdown of Aif in normal T cells.

Main Results:

  • Hq T cells showed resistance to NID but not DNA damage-induced death.
  • Aif nuclear translocation and cytochrome c release were reduced in Hq T cells during NID.
  • Hq T cells exhibited increased CD95L expression and susceptibility to AICD and hydrogen peroxide.
  • Superoxide scavenging protected wild-type but not Hq T cells from AICD.
  • siRNA reduction of Aif mimicked the altered death susceptibility in normal T cells.

Conclusions:

  • Aif plays critical, nonredundant roles in both promoting and preventing apoptosis in activated peripheral T cells.
  • Aif is implicated in regulating T cell death via cytochrome c release during NID.
  • Aif has a crucial superoxide-scavenging function in controlling T cell AICD.