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

Allergic Reactions: Anaphylaxis01:30

Allergic Reactions: Anaphylaxis

Anaphylaxis is a severe, life-threatening hypersensitivity reaction mediated by Immunoglobulin E (IgE) antibodies. When IgE binds to allergens, it triggers the release of mediators– histamine, leukotrienes, and prostaglandins from mast cells and basophils. These mediators cause vasodilation, edema, and inflammation, leading to various symptoms.The primary allergens causing anaphylaxis include food items (e.g., peanuts, shellfish), drugs (e.g., penicillin, asparaginase, corticotropin, heparin),...
Allergic Reactions02:06

Allergic Reactions

Overview
Drug Toxicity: Allergic Reactions01:30

Drug Toxicity: Allergic Reactions

Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial exposure to a...
Allergic Drug Reactions01:27

Allergic Drug Reactions

Allergic reactions related to drugs are hypersensitivity responses driven by the immune system and bear no connection to the drug's therapeutic action. While drugs in isolation do not trigger an immune response, they can interact with endogenous proteins to form antigens. These antigens stimulate lymphocytes to produce antibodies. IgE-type antibodies attach themselves to mast cells. Upon subsequent exposure to the same stimulus, the antigen-antibody interaction is initiated, unleashing numerous...
Asthma-II: Pathophysiology and Classification01:26

Asthma-II: Pathophysiology and Classification

Asthma is a prevalent chronic respiratory condition marked by inflammation and hyperresponsiveness of the airways. Its pathophysiology involves complex interactions among inflammatory pathways, immune responses, and neural mechanisms.
Additionally, environmental and genetic factors play crucial roles in determining an individual's susceptibility to asthma and the severity of their condition.
Critical processes in asthma pathophysiology include:
Asthma I: Introduction01:28

Asthma I: Introduction

Asthma is a chronic inflammatory disorder of the airways characterized by variable airflow obstruction and heightened bronchial responsiveness to a wide range of triggers. The underlying inflammation leads to airway swelling, mucus hypersecretion, and smooth muscle constriction, all of which narrow the airway lumen and impede airflow. Clinically, asthma presents with recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing, symptoms that typically vary in intensity and...

You might also read

Related Articles

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

Sort by
Same author

Molecular Characterization of Non-Specific Esophagitis Reveals a Distinct Non-Eosinophilic Phenotype With Fibrotic Traits.

Allergy·2026
Same author

An Immunologic Perspective on Adverse Reactions Observed Upon Systemic Therapies of Atopic Dermatitis: A Retrospective Study of 145 Cases.

Allergy·2026
Same author

Cytosolic proliferating cell nuclear antigen (PCNA) orchestrates neutrophil hyperactivation in COVID-19.

Proceedings of the National Academy of Sciences of the United States of America·2025
Same author

An in vivo microscopy dataset for the characterization of leukocyte death.

Scientific data·2025
Same author

Mitochondrial, metabolic and bioenergetic adaptations drive plasticity of colorectal cancer cells and shape their chemosensitivity.

Cell death & disease·2025
Same author

Comprehensive analysis of cellular metrics: From proliferation to mitochondrial membrane potential and cell death in a single sample.

Cell death discovery·2025
Same journal

Targeting the fibrosis-inflammation-oxidative stress axis: multifaceted mechanisms of salidroside in chronic organ fibrosis.

Apoptosis : an international journal on programmed cell death·2026
Same journal

Microglial tunneling nanotubes: an intercellular transfer facilitating mitochondrial dysfunction and neuroinflammation in experimental cerebral malaria.

Apoptosis : an international journal on programmed cell death·2026
Same journal

Copper dysregulation in cardiometabolic disease: copper deficiency versus cuproptosis.

Apoptosis : an international journal on programmed cell death·2026
Same journal

GPx6 downregulation drives ferroptosis in Kashin-Beck disease chondrocytes via the SLC7A11/GPx4 axis.

Apoptosis : an international journal on programmed cell death·2026
Same journal

Interplay between ischemia-reperfusion and metabolic reprogramming.

Apoptosis : an international journal on programmed cell death·2026
Same journal

CRKL amplification synergizes with mechanical stress-induced signaling to dually activate YAP oncogenic pathways, driving plantar melanoma progression.

Apoptosis : an international journal on programmed cell death·2026
See all related articles

Related Experiment Video

Updated: Jun 26, 2026

Assessment of Lymphocyte Migration in an Ex Vivo Transmigration System
10:25

Assessment of Lymphocyte Migration in an Ex Vivo Transmigration System

Published on: September 20, 2019

Cell death in allergic diseases.

Hans-Uwe Simon1

  • 1Institute of Pharmacology, University of Bern, Bern, Switzerland. hus@pki.unibe.ch

Apoptosis : an International Journal on Programmed Cell Death
|January 9, 2009
PubMed
Summary
This summary is machine-generated.

Apoptosis, a key immune process, is dysregulated in allergic diseases. Delayed leukocyte death, particularly eosinophils, contributes to inflammation, while accelerated epithelial cell death exacerbates allergic responses.

More Related Videos

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy
10:39

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy

Published on: April 16, 2019

Analysis of Pulmonary Dendritic Cell Maturation and Migration during Allergic Airway Inflammation
07:52

Analysis of Pulmonary Dendritic Cell Maturation and Migration during Allergic Airway Inflammation

Published on: July 23, 2012

Related Experiment Videos

Last Updated: Jun 26, 2026

Assessment of Lymphocyte Migration in an Ex Vivo Transmigration System
10:25

Assessment of Lymphocyte Migration in an Ex Vivo Transmigration System

Published on: September 20, 2019

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy
10:39

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy

Published on: April 16, 2019

Analysis of Pulmonary Dendritic Cell Maturation and Migration during Allergic Airway Inflammation
07:52

Analysis of Pulmonary Dendritic Cell Maturation and Migration during Allergic Airway Inflammation

Published on: July 23, 2012

Area of Science:

  • Immunology
  • Cell Biology
  • Pathology

Background:

  • Apoptosis (programmed cell death) is crucial for immune system regulation.
  • Caspases, intracellular proteases, control apoptosis and are regulated by anti-apoptotic molecules.
  • Leukocyte apoptosis rates are influenced by survival factors and change under pathological conditions.

Purpose of the Study:

  • To review the regulation of leukocyte lifespan in allergic inflammatory responses.
  • To highlight the role of deregulated cell death in allergic disease pathogenesis.
  • To discuss how altered apoptosis contributes to immune cell accumulation and inflammation.

Main Methods:

  • Literature review of studies on apoptosis and allergic inflammation.
  • Analysis of mechanisms regulating leukocyte survival and death pathways.
  • Examination of the role of caspases and anti-apoptotic molecules in immune cells.

Main Results:

  • Allergic diseases exhibit deregulated cell death, with delayed apoptosis in leukocytes like eosinophils, leading to eosinophilia.
  • Accelerated apoptosis in epithelial cells can amplify allergic inflammation.
  • Survival factor expression is often elevated in inflammation, promoting immune cell survival.

Conclusions:

  • Dysregulated apoptosis is a common feature and likely contributor to the pathogenesis of allergic diseases.
  • The balance of apoptosis (too little or too much) is cell-type dependent.
  • Understanding leukocyte lifespan regulation is key to addressing allergic inflammatory responses.