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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...
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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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Receptor tyrosine kinases or RTKs are membrane-bound receptors that phosphorylate specific tyrosine on protein substrates. RTKs regulate cellular growth, differentiation, survival, and migration. They contain an extracellular ligand binding domain, a transmembrane domain, and a cytosolic tail with intrinsic kinase activity. Several extracellular signaling molecules activate RTKs in one or more ways and relay the signal downstream. Ligands such as platelet-derived growth factor (PDGF) or...
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Related Experiment Video

Updated: May 16, 2026

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

Published on: May 3, 2024

TLR activation regulates damage-associated molecular pattern isoforms released during pyroptosis.

Sanna Nyström1, Daniel J Antoine, Peter Lundbäck

  • 1Department of Medicine, Center for Infectious Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.

The EMBO Journal
|December 11, 2012
PubMed
Summary

Pyroptosis, a form of cell death, does not require priming. Unprimed pyroptosis releases damage-associated molecular patterns (DAMPs) like HMGB1, independent of inflammatory signaling or mitochondrial involvement.

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Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages

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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
  • Cell Biology
  • Microbiology

Background:

  • Bacterial infections activate Toll-like receptors (TLRs) and Nod-like receptors (NLRs) in macrophages, leading to inflammasome activation and pyroptosis.
  • Priming is a complex process that complicates the study of inflammasome activation and pyroptosis.

Purpose of the Study:

  • To develop a priming-free NLRC4 inflammasome activation system.
  • To investigate the necessity and role of priming in pyroptotic cell death and damage-associated molecular pattern (DAMP) release.

Main Methods:

  • Development of a priming-free NLRC4 inflammasome activation system in macrophages.
  • Analysis of pyroptosis, DAMP release, cytokine production, nitrous oxide (NO), and reactive oxygen species (ROS) with and without priming.

Main Results:

  • Pyroptosis is not dependent on priming and is unaffected by its re-introduction.
  • Unprimed pyroptosis is independent of mitochondrial involvement and does not produce inflammatory cytokines, NO, or ROS.
  • Unprimed pyroptosis releases high mobility group protein box 1 (HMGB1), a DAMP.
  • Priming via surface TLRs, but not endosomal TLRs, during pyroptosis leads to the release of a TLR4-agonist cysteine redox isoform of HMGB1.

Conclusions:

  • Pyroptosis is dominant to priming signals.
  • Metabolic changes induced by priming can influence the immune system's perception of cell death.
  • The study reveals distinct HMGB1 isoforms released during pyroptosis depending on priming status.