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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),...

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Updated: Jun 1, 2026

Measuring Local Anaphylaxis in Mice

Measuring Local Anaphylaxis in Mice

Published on: October 14, 2014

Pathophysiology of anaphylaxis.

Bilal Q Khan¹, Stephen F Kemp

¹Division of Clinical Immunology and Allergy, Department of Medicine, The University of Mississippi Medical Center, Jackson, Mississippi 39216, USA.

Current Opinion in Allergy and Clinical Immunology

|June 11, 2011

Summary

This summary is machine-generated.

This review explores the complex pathophysiology of anaphylaxis, including traditional and alternative pathways. Understanding these mechanisms, including compensatory responses, is key for future diagnosis and management strategies.

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Last Updated: Jun 1, 2026

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Area of Science:

Immunology
Allergy
Pathophysiology

Background:

Anaphylaxis pathophysiology traditionally centers on IgE-dependent and IgE-independent mediator release from mast cells and basophils.
Emerging research highlights the importance of alternative pathways in anaphylaxis.
Internal compensatory mechanisms activated during anaphylaxis are gaining research attention.

Purpose of the Study:

To provide a comprehensive overview of the current understanding of anaphylaxis pathophysiology.
To discuss the evolving knowledge regarding the mechanisms underlying anaphylaxis.
To highlight recent advancements in the field.

Main Methods:

Review of current scientific literature.
Synthesis of data on immunopathologic mechanisms.
Analysis of emerging research on alternative pathways and compensatory responses.

Main Results:

Traditional models of anaphylaxis involve IgE-dependent and IgE-independent mast cell and basophil degranulation.
Evidence is accumulating for the involvement of alternative pathways in the development of anaphylaxis.
Internal regulatory and compensatory mechanisms play a significant role in the anaphylactic response.

Conclusions:

Recent scientific advances are deepening the understanding of anaphylaxis pathophysiology.
This enhanced understanding holds potential for future improvements in anaphylaxis diagnosis.
Future implications for the clinical management of anaphylaxis are anticipated.