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Allergic Reactions: Anaphylaxis

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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,...

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Related Experiment Video

Updated: Mar 26, 2026

Investigating Mast Cell Secretory Granules; from Biosynthesis to Exocytosis

Investigating Mast Cell Secretory Granules; from Biosynthesis to Exocytosis

Published on: January 26, 2015

Mast Cells and Anaphylaxis.

Phil Lieberman^1,2, Lene Heise Garvey³

¹Divisions of Allergy and Immunology, Departments of Medicine and Pediatrics, University of Tennessee, Memphis, TN, USA. aac@allergymemphis.com.

Current Allergy and Asthma Reports

|February 10, 2016

Summary

This summary is machine-generated.

Mast cells mediate anaphylaxis through various triggers. Recent findings suggest the MRGPRX2 receptor may be key in drug-induced anaphylactic events, independent of IgE.

Keywords:

Anaphylaxis Basophil Immunoglobulin E MRGPRX2 Mast cell Mast cell mediators Mast cell secretagogues Tryptase

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Last Updated: Mar 26, 2026

Investigating Mast Cell Secretory Granules; from Biosynthesis to Exocytosis

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Published on: January 26, 2015

Measuring Local Anaphylaxis in Mice

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An Ex vivo Mast Cell Degranulation Assay using Crude Peritoneal Exudate Cells and Natural Antigen Stimulation

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Published on: April 27, 2021

Area of Science:

Immunology
Cell Biology
Pharmacology

Background:

Mast cells are central to anaphylaxis, releasing mediators that cause clinical symptoms.
Immunoglobulin E (IgE) was initially thought to be the primary trigger for anaphylactic episodes via antigen binding.
Recent research indicates mast cell activation can occur independently of IgE-antigen interactions.

Purpose of the Study:

To explore mechanisms of mast cell activation beyond IgE-dependent pathways.
To investigate the role of novel receptors in direct mast cell degranulation.
To identify potential targets for managing anaphylactic events.

Main Methods:

Review of existing literature on mast cell activation and anaphylaxis.
Analysis of recent reports on G-protein-coupled receptors involved in mast cell degranulation.
Focus on antigen-independent mast cell activation pathways.

Main Results:

Mast cells release mediators responsible for anaphylactic manifestations.
Direct mast cell activation, not involving IgE, accounts for many anaphylactic episodes.
Monomeric IgE can also induce mast cell degranulation under specific conditions.

Conclusions:

The MRGPRX2 receptor, a G-protein-coupled receptor, is implicated in direct mast cell degranulation.
This receptor may mediate anaphylactic events triggered by various drugs and cationic proteins.
Understanding MRGPRX2 is crucial for elucidating non-IgE-dependent anaphylaxis mechanisms.