Related Experiment Video

Updated: Jan 25, 2026

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

3.8K

Death Receptor Interactions With the Mitochondrial Cell Death Pathway During Immune Cell-, Drug- and Toxin-Induced

Valentina Spinnenhirn1, Janine Demgenski1, Thomas Brunner1

  • 1Biochemical Pharmacology, Department of Biology, University of Konstanz, Konstanz, Germany.

Frontiers in Cell and Developmental Biology
|May 10, 2019
PubMed

Insights

The liver faces constant threats from toxins and infections. This study explores how immune cells and specific signaling pathways regulate drug-induced liver injury, focusing on cell death mechanisms.

Area of Science:

  • Hepatology
  • Immunology
  • Toxicology

Background:

  • The liver's vital functions expose it to xenobiotics, necessitating detoxification pathways.
  • Drug metabolism can generate toxic byproducts, leading to liver damage and immune activation.
  • Understanding immune cell roles in drug-induced liver injury (DILI) is crucial.

Purpose of the Study:

  • To investigate the role of immune cells and effector molecules in DILI.
  • To elucidate the mechanisms of xenobiotic-induced liver damage.
  • To explore the interplay between death receptor (DR) and mitochondrial pathways in DILI.

Main Methods:

  • Discussion of TNF family members, particularly TRAIL (TNF-related apoptosis-inducing ligand).
  • Analysis of interactions between TNF family and Bcl-2 family proteins.
  • Examination of crosstalk between extrinsic and intrinsic cell death pathways.

Main Results:

  • Hepatocytes utilize mitochondrial pathways for death receptor-induced cell death (CD).
  • Mitochondria are implicated in drug-induced activation of cell death pathways.
  • TNF family members, like TRAIL, play a role in regulating DILI.

Conclusions:

  • Immune cell involvement is critical in managing drug-induced liver damage.
  • The interplay between extrinsic and intrinsic cell death pathways is central to DILI.
  • TRAIL and Bcl-2 family interactions are key mediators in xenobiotic-induced liver injury.
Keywords:
APAPBcl2 familyBimDILIJNKTRAILdeath receptor

More Related Videos

Author Spotlight: Understanding Cytokine-Induced Cell Death in Intestinal Epithelial Cells Using Human Organoids10:03

Author Spotlight: Understanding Cytokine-Induced Cell Death in Intestinal Epithelial Cells Using Human Organoids

Published on: August 2, 2024

2.0K
Studying Copper Nanoparticle-Induced Programmed Cell Death in Bacteria08:22

Studying Copper Nanoparticle-Induced Programmed Cell Death in Bacteria

Published on: May 16, 2025

563

Related Concept Videos

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...
9.6K
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
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
4.4K
Drug-Receptor Interactions01:29

Drug-Receptor Interactions

Drug-receptor interaction describes the binding of receptors by drugs, but not all drug-receptor interactions result in activation and tissue response. For instance, the binding of agonists activates the receptor to generate a cellular reaction, while antagonists bind to receptors without causing their activation.
Several parameters, such as the drug's affinity for its receptor and its efficacy, which is its ability to activate the receptor, determine the drug's effect on the tissue....
7.4K
Drug-Receptor Interaction: Antagonist01:28

Drug-Receptor Interaction: Antagonist

An antagonist is a drug that binds strongly to a receptor without activating it. An antagonist prevents other molecules, such as neurotransmitters or hormones, from binding to the receptor and triggering a cellular response. Such interaction effectively hinders the normal physiological processes mediated by the receptor, resulting in various pharmacological effects depending on the specific receptor targeted.
Antagonists can be classified as competitive or noncompetitive based on their...
5.0K
Drug-Receptor Interaction: Agonist01:25

Drug-Receptor Interaction: Agonist

Agonists are drugs that interact with specific receptors in the body to produce a biological response. When an agonist binds to a receptor, it activates or enhances the receptor's function, leading to physiological effects. The interaction between agonist drugs and receptors is crucial for their therapeutic action in various medical treatments.
Agonists can bind to receptors in different ways. Some agonists bind directly to the receptor's active site, mimicking the endogenous...
4.1K
Quantitative Aspects of Drug-Receptor Interaction01:30

Quantitative Aspects of Drug-Receptor Interaction

The receptor occupancy theory connects a drug's response to the number of occupied receptors. With higher drug concentrations, more receptors are occupied, leading to increased responses. The formation of drug-receptor complexes involves association and dissociation rates, which reach equilibrium when the forward and backward reactions are equal. The equilibrium association constant (Ka) and its inverse, the equilibrium dissociation constant (Kd), indicate drug affinity. Higher Ka and lower...
1.7K