Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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...
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...
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...
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...
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.
Cellular Injury IlI: Cellular Death01:11

Cellular Injury IlI: Cellular Death

Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Eosinophilia Reflects Type 2 Immune Activation in Newly Diagnosed Bullous Pemphigoid, With No Evidence of Charcot-Leyden Crystals.

Allergy·2026
Same author

Declining venom immunotherapy: patient characteristics and clinical outcomes.

Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology·2026
Same author

Clinical pearl: Topical Lactobacillus application to disrupt Pseudomonas aeruginosa biofilms and promote healing in chronic wounds.

Journal of the American Academy of Dermatology·2025
Same author

High Prevalence of Metabolic Dysfunction-Associated Steatotic Liver Disease in Patients with Hidradenitis Suppurativa: A Guide to Easily Assess the Clinical Risk of Comorbid Liver Disease.

JID innovations : skin science from molecules to population health·2025
Same author

NFATc1 Abrogation in B Cells Ameliorates Contact Hypersensitivity Responses.

International journal of molecular sciences·2025
Same author

Recommendations on how to proceed in case of suspected allergy to penicillin/β-lactam antibiotics: Position paper of the German Society for Allergology and Clinical Immunology (DGAKI) in cooperation with the German Society for Pediatric Allergology (GPA), Austrian Society for Allergology and Immunology (ÖGAI) and the Swiss Society for Allergology and Immunology (SGAI).

Allergologie select·2025

Related Experiment Video

Updated: Jun 21, 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

Effector pathways during eczematous dermatitis: where inflammation meets cell death.

Andreas Kerstan1, Martin Leverkus, Axel Trautmann

  • 1Department of Dermatology, Venerology and Allergology, University of Würzburg, Germany.

Experimental Dermatology
|July 16, 2009
PubMed
Summary

Skin inflammation in eczema involves keratinocyte-T cell interactions. Damaged keratinocytes trigger further immune responses, highlighting the need to understand these mechanisms for new eczema therapies.

More Related Videos

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Related Experiment Videos

Last Updated: Jun 21, 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

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Area of Science:

  • Immunology
  • Dermatology
  • Cell Biology

Background:

  • Eczematous skin inflammation involves complex interactions between skin cells and immune cells.
  • Keratinocytes (KC) are crucial in initiating and modulating immune responses to environmental triggers.
  • A disturbed skin barrier function is a key factor in eczematous dermatitis.

Purpose of the Study:

  • To review the epidermal inflammation driven by keratinocyte-T cell interactions in eczema.
  • To elucidate the mechanisms of keratinocyte apoptosis and inflammatory mediator secretion.
  • To discuss potential therapeutic strategies targeting these pathways.

Main Methods:

  • Review of existing literature on eczematous dermatitis pathogenesis.
  • Analysis of keratinocyte-T cell interactions in epidermal inflammation.
  • Discussion of immunoregulatory mechanisms and therapeutic targets.

Main Results:

  • Eczematous dermatitis is characterized by T cells inducing keratinocyte apoptosis.
  • Damaged keratinocytes release inflammatory mediators, recruiting more immune cells.
  • The interplay between keratinocytes and T cells exacerbates skin inflammation.

Conclusions:

  • Understanding keratinocyte-T cell interactions is vital for advancing eczema treatment.
  • Identifying specific immunoregulatory mechanisms offers therapeutic potential.
  • Targeting these pathways may lead to novel interventions for eczematous dermatitis.