Atopy and Role of Mast Cells in IgE-Mediated Allergic Diseases

ISSN: 1875-631X (Online)
ISSN: 1573-3955 (Print)


Volume 10, 2 Issues, 2014


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Current Immunology Reviews

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Editor-in-Chief:
Cecil Czerkinsky
Institut de Pharmacologie Moleculaire et Cellulaire
UMR 7275 CNRS-INSERM-UNISA
660 Route des Lucioles
Valbonne, 06560
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Atopy and Role of Mast Cells in IgE-Mediated Allergic Diseases

Author(s): Guillermina Yanek Jiménez-Andrade

Affiliation: Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA.

Abstract

Atopy is characterized by a high production of IgE in response to common allergens exposure and by positive responses to skin-prick test against specific antigens. Atopy can contribute to the development of atopic asthma and atopic eczema. This condition involves the participation of different cells including mast cells that express the high-affinity Fc receptor for IgE, the FcεRI receptor. Crosslinking of FcεRI-bound IgE in absence of an allergen increases the expression of IgE receptor, enhances mast cells survival and induces synthesis and secretion of several inflammatory mediators that contribute to increase allergic reactions. The number of mast cells and their mediators increase in asthma and eczema and could be involved in the pathogenesis of these diseases.

Genetic factors such as mutations and polymorphism in several genes of the subunits of the FcεRI (receptor for IgE), cytokines and their receptors (IL-4, IL-13), and transcription factors (STAT6) allow IgE synthesis. Moreover, epigenetic regulation of genes such as DNA methylation and histone modifications are the genetic background of atopy.

This review attempts to summarize the recent progress on the pathology of atopy, its risk factors and the role of mast cells in two atopic diseases: atopic asthma and atopic eczema.


Keywords: Atopy, atopic asthma, atopic eczema, FcεRI, IgE, inflammatory mediators, mast cells.

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Article Details

Volume: 9
Issue Number: 4
First Page: 249
Last Page: 260
Page Count: 12
DOI: 10.2174/1573395510666140305000155
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