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 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...
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...
Hypersensitivity Reactions: Delayed Hypersensitivity Reactions01:29

Hypersensitivity Reactions: Delayed Hypersensitivity Reactions

Delayed-Type Hypersensitivity (DTH), or Type IV hypersensitivity, is a cell-mediated immune response. It occurs when T cells, rather than antibodies, mediate a reaction to specific antigens. It is characterized by a delayed onset (1-2 days) and involves the recruitment of macrophages to the inflammation site.The initiation of a DTH response begins with the sensitization of T cells. During this phase, which lasts at least 1-2 weeks, antigen-specific T cells are activated, clonally expanded, and...
Acute Inflammation I: Inflammatory Response01:26

Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...

You might also read

Related Articles

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

Sort by
Same author

Leukocyte activation and the asthmatic response.

Immunology today·2014
Same author

Chronic urticaria/angioedema and Graves' disease: Coexistence of 2 antireceptor antibody-mediated diseases.

The Journal of allergy and clinical immunology·2001
Same author

ICOS ligand costimulation is required for T-cell encephalitogenicity.

Clinical immunology (Orlando, Fla.)·2001
Same author

Quantitative comparison of cytokine mRNA and inflammatory responses in cutaneous late phase allergic reactions.

Cytokine·2000
Same author

Sequential patterns of inflammatory events during developing and expressed skin late-phase reactions.

The Journal of allergy and clinical immunology·2000
Same author

Comparative effects of antilactoferrin antibodies and tumor necrosis factor on neutrophil adherence to matrix proteins.

Clinical and diagnostic laboratory immunology·1999

Related Experiment Video

Updated: Jul 1, 2026

Absorption of Nasal and Bronchial Fluids: Precision Sampling of the Human Respiratory Mucosa and Laboratory Processing of Samples
11:54

Absorption of Nasal and Bronchial Fluids: Precision Sampling of the Human Respiratory Mucosa and Laboratory Processing of Samples

Published on: January 21, 2018

Temporal patterns of mediator release during developing cutaneous late-phase reactions.

B Zweiman1, C Von Allmen

  • 1Department of Medicine, Division of Allergy and Immunology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.

Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology
|June 10, 2000
PubMed
Summary

Cutaneous late phase reactions involve rapid inflammatory mediator release and immune cell activation. Histamine, lactoferrin, and eosinophil cationic protein are released early, contributing to skin inflammation.

More Related Videos

Precision Implementation of Minimal Erythema Dose (MED) Testing to Assess Individual Variation in Human Inflammatory Response
06:31

Precision Implementation of Minimal Erythema Dose (MED) Testing to Assess Individual Variation in Human Inflammatory Response

Published on: October 3, 2019

Humanized Mediator Release Assay as a Read-Out for Allergen Potency
10:22

Humanized Mediator Release Assay as a Read-Out for Allergen Potency

Published on: June 29, 2021

Related Experiment Videos

Last Updated: Jul 1, 2026

Absorption of Nasal and Bronchial Fluids: Precision Sampling of the Human Respiratory Mucosa and Laboratory Processing of Samples
11:54

Absorption of Nasal and Bronchial Fluids: Precision Sampling of the Human Respiratory Mucosa and Laboratory Processing of Samples

Published on: January 21, 2018

Precision Implementation of Minimal Erythema Dose (MED) Testing to Assess Individual Variation in Human Inflammatory Response
06:31

Precision Implementation of Minimal Erythema Dose (MED) Testing to Assess Individual Variation in Human Inflammatory Response

Published on: October 3, 2019

Humanized Mediator Release Assay as a Read-Out for Allergen Potency
10:22

Humanized Mediator Release Assay as a Read-Out for Allergen Potency

Published on: June 29, 2021

Area of Science:

  • Immunology
  • Dermatology
  • Allergy Research

Background:

  • Cutaneous late phase reactions (LPR) involve inflammatory mediators.
  • The precise timing of mediator release during LPR development remains unclear.

Purpose of the Study:

  • To chronologically map mediator release during LPR.
  • To correlate mediator release with inflammatory cell responses and gross LPR development.

Main Methods:

  • Utilized skin chambers for hourly sample collection following allergen challenge.
  • Analyzed exuded leukocytes for activation and mediator content.

Main Results:

  • Histamine release peaked within the first hour post-allergen challenge.
  • Neutrophil-derived lactoferrin and eosinophil cationic protein release followed, associated with IL-8.
  • A higher percentage of activated leukocytes was observed in allergen-challenged sites.

Conclusions:

  • Skin inflammatory responses, including leukocyte activation and mediator release, commence shortly after initial mast cell activation in IgE-mediated reactions.
  • These findings elucidate the temporal dynamics of LPR development.