Cited by 350Dermatology and Skin DiseasesContact Dermatitis and AllergiesSkin and Cellular Biology Research

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Filaggrin in atopic dermatitis

O'Regan, Grainne M., Sandilands, Aileen, McLean, W.H. Irwin, Irvine, Alan D.·2008·Journal of Allergy and Clinical Immunology

DOI 10.1016/j.jaci.2008.08.002

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Abstract

The recent identification of loss-of-function mutations in the structural protein filaggrin as a widely replicated major risk factor for eczema sheds new light on disease mechanisms in eczema, a disease that had heretofore largely been considered to have a primarily immunologic etiopathogenesis. The filaggrin gene (FLG) mutation findings are consistent with a recently proposed unifying hypothesis that offers a mechanistic understanding of eczema pathogenesis synthesizing a heritable epithelial barrier defect and resultant diminished epidermal defense mechanisms to allergens and microbes, followed by polarized T(H)2 lymphocyte responses with resultant chronic inflammation, including autoimmune mechanisms. Although compelling evidence from genetic studies on FLG implicates perturbed barrier function as a key player in the pathogenesis of eczema in many patients, much is still unknown about the sequence of biologic, physicochemical, and aberrant regulatory events that constitute the transition from an inherited barrier defect to clinical manifestations of inflammatory eczematous lesions and susceptibility to related atopic disorders. The exact contribution of FLG to the wider atopic story, factors modifying FLG expression, and the role of other barrier proteins remain to be delineated. In this review we highlight recent advances in our understanding of the FLG genetics in the cause of eczema and related complex diseases.

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Authors: O'Regan, G. M., Sandilands, A., McLean, W. H. I., & Irvine, A. D.
Affiliations: University of Dundee (GB)
Trinity College Dublin (IE)
Corresponding author: Irvine, Alan D.
ORCID: Sandilands, Aileen
McLean, W.H. Irwin
Irvine, Alan D.
Venue: Journal of Allergy and Clinical Immunology
Publisher: Elsevier BV
Published: 2008-10
Volume: 122
Issue: 4
Pages: 689-693
ISSN: 0091-6749 (ISSN-L)
DOI: 10.1016/j.jaci.2008.08.002
OpenAlex: W4296927509
Cited by: 350
References: 25
Citations by year: 2026: 8 · 2025: 6 · 2024: 13 · 2023: 14 · 2022: 20 · 2021: 20 · 2020: 29 · 2019: 22 · 2018: 9 · 2017: 15 · 2016: 14 · 2015: 11 · 2014: 17 · 2013: 23 · 2012: 25
FWCI: 37.11
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Journal of Allergy and Clinical Immunology (publishedVersion)
PubMed (publishedVersion)
Discovery Research Portal (University of Dundee) (publishedVersion)
Topics: Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
Health Sciences › Medicine › Dermatology › Contact Dermatitis and Allergies
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Skin and Cellular Biology Research
Keywords: filaggrin, FLG gene, atopic dermatitis, loss-of-function mutations, epithelial barrier function, chronic inflammation, autoimmune mechanisms, atopic diseases, genetic susceptibility
MeSH terms: Filaggrin Proteins, Animals, Chronic Disease, Dermatitis, Atopic, Eczema, Flagellin, Humans, Inflammation, Mutation, Autoimmunity, Th2 Cells

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Filaggrin in atopic dermatitis

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