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Allergic Reactions

Allergic Reactions

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...

Cross-reactivity

Cross-reactivity

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...

Allergic Reactions: Anaphylaxis

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),...

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...

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Updated: May 19, 2026

Removal and Replacement of Endogenous Ligands from Lipid-Bound Proteins and Allergens

Removal and Replacement of Endogenous Ligands from Lipid-Bound Proteins and Allergens

Published on: February 24, 2021

Interactions between FLG mutations and allergens in atopic dermatitis.

Ming Li¹, Jiang-Bo Liu, Qiang Liu

¹Department of Dermatology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

Archives of Dermatological Research

|August 21, 2012

Summary

Filaggrin gene (FLG) mutations interact with peanut sensitization in atopic dermatitis (AD) patients. This interaction is specifically linked to the K4671X mutation and combined FLG mutations, influencing AD development.

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Removal and Replacement of Endogenous Ligands from Lipid-Bound Proteins and Allergens

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Published on: June 29, 2021

Area of Science:

Genetics
Immunology
Dermatology

Background:

Filaggrin gene (FLG) mutations are common in atopic dermatitis (AD).
Sensitization to specific allergens is a hallmark of AD.
The interplay between FLG mutations and allergen sensitization in AD remains unclear.

Purpose of the Study:

To investigate the interaction between FLG mutations and specific allergen sensitization in AD patients.
To identify specific allergens that interact with FLG mutations in the context of AD.

Main Methods:

Recruited 249 AD outpatients.
Performed skin prick tests for allergen sensitization.
Conducted comprehensive FLG gene sequencing.
Utilized logistic regression analysis to assess interactions.

Main Results:

FLG mutations were identified in 64 patients (25.7%).
Specific mutations 3321delA and K4671X were found in 9.6% and 11.6% of cases, respectively.
47.4% of patients showed sensitization to at least one allergen.
FLG mutations interacted with peanut sensitization, particularly the K4671X mutation and combined mutations.

Conclusions:

FLG mutations interact with peanut sensitization in AD patients.
This interaction, especially with K4671X and combined mutations, may play a role in AD pathogenesis.
Sensitization to other common allergens may not interact with FLG mutations in AD development.