Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Allergic Drug Reactions

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...

Hypersensitivities

Hypersensitivities

Hypersensitivity, also known as a hypersensitivity reaction or allergic reaction, is a condition where the body's immune system reacts abnormally to a foreign substance. Such substances, that cause hypersensitivity are referred to as an allergen, could be something typically harmless to most people, like pollen or certain foods.
Types of Hypersensitivities
Hypersensitivity reactions are categorized into four types: Type 1, Type 2, Type 3, and Type 4. Each type has a distinct mechanism...

Drug Toxicity: Allergic Reactions

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: Cytolytic Reactions

Hypersensitivity Reactions: Cytolytic Reactions

Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...

Hypersensitivity Reactions: Delayed Hypersensitivity Reactions

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...

Hypersensitivity Reactions: Immune-Complex Reactions

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

Allergic contact dermatitis in children: a practical approach to management.

Skin therapy letter·2003

Same author

Tumors arising in nevus sebaceus.

Journal of the American Academy of Dermatology·2001

Same author

What syndrome is this? Ehlers-Danlos syndrome.

Pediatric dermatology·2001

Same author

Kwashiorkor in the United States: fad diets, perceived and true milk allergy, and nutritional ignorance.

Archives of dermatology·2001

Same author

Unsuspected sporotrichosis in childhood.

The Pediatric infectious disease journal·2001

Same author

Beyond poison ivy: understanding allergic contact dermatitis in children.

Pediatric annals·2001

Search research articles

Related Experiment Video

Updated: Jun 28, 2026

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis

Published on: December 15, 2011

Type IV reactions in the skin

Annals of Allergy

|November 1, 1976

Summary

Allergic eczematous contact dermatitis (AECD) is a Type IV hypersensitivity reaction mediated by T lymphocytes. It involves sensitization via haptens binding to proteins, with diagnosis confirmed by patch testing and treatment with corticosteroids.

Area of Science:

Immunology
Dermatology

Background:

Delayed type (Type IV) hypersensitivity commonly presents as allergic eczematous contact dermatitis (AECD).
This immune response is mediated by T lymphocytes and can be transferred via lymphoid cells.
The sensitization phase correlates with in vitro lymphocyte transformation, and the elicitation phase with lymphokine activity.

Purpose of the Study:

To summarize the understanding of allergic eczematous contact dermatitis (AECD).
To highlight the immunological mechanisms and diagnostic approaches for AECD.

Main Methods:

Review of existing evidence correlating sensitization and elicitation phases of AECD.
Discussion of the role of haptens and protein binding in AECD pathogenesis.
Emphasis on diagnostic patch testing and therapeutic interventions.

More Related Videos

A Suction Blister Protocol to Study Human T-cell Recall Responses In Vivo

A Suction Blister Protocol to Study Human T-cell Recall Responses In Vivo

Published on: August 11, 2018

A Standardized Procedure of Dressing Management for Toxic Epidermal Necrolysis

A Standardized Procedure of Dressing Management for Toxic Epidermal Necrolysis

Published on: March 14, 2025

Related Experiment Videos

Last Updated: Jun 28, 2026

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis

Published on: December 15, 2011

A Suction Blister Protocol to Study Human T-cell Recall Responses In Vivo

A Suction Blister Protocol to Study Human T-cell Recall Responses In Vivo

Published on: August 11, 2018

A Standardized Procedure of Dressing Management for Toxic Epidermal Necrolysis

A Standardized Procedure of Dressing Management for Toxic Epidermal Necrolysis

Published on: March 14, 2025

Main Results:

A bewildering variety of haptens can cause AECD, all capable of forming covalent bonds with proteins.
Patch testing with the causative antigen reliably reproduces the condition.
Lymphocyte transformation and lymphokine activity are key components of the immune response.

Conclusions:

Allergic eczematous contact dermatitis is a T lymphocyte-mediated hypersensitivity reaction.
Diagnosis relies on identifying the offending hapten via patch testing.
Topical or systemic corticosteroids are the primary treatment modality for AECD.