Cited by 1,799Mast cells and histamineAsthma and respiratory diseasesAllergic Rhinitis and Sensitization

IgE and mast cells in allergic disease

Open access
Galli, Stephen J, Tsai, Mindy·2012·Nature Medicine

Abstract

Immunoglobulin E (IgE) antibodies and mast cells have been so convincingly linked to the pathophysiology of anaphylaxis and other acute allergic reactions that it can be difficult to think of them in other contexts. However, a large body of evidence now suggests that both IgE and mast cells are also key drivers of the long-term pathophysiological changes and tissue remodeling associated with chronic allergic inflammation in asthma and other settings. Such potential roles include IgE-dependent regulation of mast-cell functions, actions of IgE that are largely independent of mast cells and roles of mast cells that do not directly involve IgE. In this review, we discuss findings supporting the conclusion that IgE and mast cells can have both interdependent and independent roles in the complex immune responses that manifest clinically as asthma and other allergic disorders.

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Crossref · 10.1038/nm.2755

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  • The severity of MCA correlates with the extent of mediator release from MC during an anaphylactic reaction.

    “the severity of MCA correlates with the extent of mediator release from MC during an anaphylactic reaction.”

    From Proposed Diagnostic Algorithm for Patients with Suspected Mast Cell Activation Syndrome (2019) · cites this paper as [5]

    The section “IgE and mast cells mediate an immediate hypersensitivity response” (page unavailable) says that mast-cell mediators induce an immediate reaction that can become anaphylaxis when systemic. It does not say that the severity of mast-cell activation correlates with the extent of mediator release during an anaphylactic reaction. (LLM, conf=0.82)

    Experimental — accuracy not yet measured
  • MCA symptoms are caused by vasoactive and pro-inflammatory mediators released from MC upon activation by allergen via IgER cross-linking or other mechanisms.

    “MCA symptoms are caused by several different vasoactive and pro-inflammatory mediators released from MC when these cells are activated by an allergen via IgER cross-linking or other mechanisms (1-5,29-31).”

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Authors
Galli, S. J., & Tsai, M.
Affiliations
Stanford Medicine (US)
Corresponding author
Galli, Stephen J
Venue
Nature Medicine
Published
2012-05
Volume
18
Issue
5
Pages
693-704
ISSN
  • 1078-8956 (ISSN-L)
  • 1546-170X
OpenAlex
W1982386486
Cited by
1,799
References
172
Citations by year
2026: 91 · 2025: 132 · 2024: 125 · 2023: 138 · 2022: 153 · 2021: 204 · 2020: 184 · 2019: 152 · 2018: 132 · 2017: 116 · 2016: 98 · 2015: 96 · 2014: 93 · 2013: 67 · 2012: 14
FWCI
7.96
Type
journal article
Language
en
Open access
Locations
  • Nature Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Cancer Institute (R01CA072074, CA 72074)
  • National Institute of Allergy and Infectious Diseases (AI-070813, R01AI023990, R01AI070813, R37AI023990, AI-23990)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
  • Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
  • Health Sciences › Medicine › Immunology and Allergy › Allergic Rhinitis and Sensitization
Keywords
immunoglobulin E, mast cells, asthma, allergic diseases, chronic allergic inflammation, tissue remodeling, anaphylaxis, asthma pathophysiology, asthma treatment
MeSH terms
Allergens, Animals, Humans, Hypersensitivity, Immunoglobulin E, Mast Cells, Receptors, IgE

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