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Overview of Cell Death01:30

Overview of Cell Death

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.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
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 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...
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...
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...

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Related Experiment Video

Updated: Jun 18, 2026

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
06:12

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

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Structure and function of programmed death (PD) molecules.

A Folkl1, D Bienzle

  • 1Department of Pathobiology, University of Guelph, Guelph, ON N1G 2W1, Canada.

Veterinary Immunology and Immunopathology
|November 26, 2009
PubMed
Summary

Programmed death-1 (PD-1) and its ligand PD-L1 are key regulators of adaptive immunity. Their interaction inhibits T-cell responses, crucial for immune tolerance and managing infections.

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Last Updated: Jun 18, 2026

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Published on: May 3, 2024

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Evaluation of Caspase Activation to Assess Innate Immune Cell Death
10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

Area of Science:

  • Immunology
  • Molecular Biology
  • Cellular Signaling

Background:

  • Programmed death (PD) molecules, part of the B7 family, regulate adaptive immunity.
  • PD-1 (CD279) is found on lymphocytes and macrophages, while its ligand PD-L1 (CD274) is expressed on immune and non-hematopoietic cells.

Purpose of the Study:

  • To elucidate the role of PD-1 and PD-L1 interactions in adaptive immunity.
  • To understand the molecular mechanisms underlying PD-1 mediated T-cell inhibition.

Main Methods:

  • Analysis of PD-1 and PD-L1 expression patterns.
  • Investigation of signaling pathways downstream of PD-1 ligation, including phosphorylation events.
  • Assessment of T-cell responses following PD-1/PD-L1 engagement.

Main Results:

  • PD-1/PD-L1 ligation inhibits T-cell proliferation, cytokine production, and cytolytic function.
  • This inhibition occurs via phosphorylation of immunoreceptor tyrosine-based switch motifs and blockade of T cell receptor signaling.
  • PD-1 and PD-L1 interactions are critical for maintaining peripheral immune tolerance.

Conclusions:

  • PD-1/PD-L1 pathway is essential for regulating T-cell activation and preventing autoimmunity.
  • Dysregulation of PD-1/PD-L1 expression is implicated in autoimmune diseases and chronic viral infections.