Association of polymorphisms in the promoter region of FCER1A gene with atopic dermatitis, chronic uticaria, asthma, and serum immunoglobulin E levels in a Han Chinese population

Zhou, Juan; Zhou, Ying; Lin, Lihui; Wang, Juan; Xia, Peng; Li, Jia; Li, Li

doi:10.1016/j.humimm.2011.12.001

Cited by 21 publications

(22 citation statements)

References 25 publications

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“…A haplotype variant of the histamine 4 receptor (H4R) and a copy number variation were found to be associated with AD [72,73]. An SNP of FCER1A was reported to be associated with AD in Asians with an elevated serum IgE level [74,75,76]. The T allele of brain-derived neurotrophic factor gene polymorphism in C270T is associated with intrinsic AD and male sex.…”

Section: Geneticsmentioning

confidence: 99%

Molecular Mechanisms of Cutaneous Inflammatory Disorder: Atopic Dermatitis

Kim

Cho

et al. 2016

IJMS

106

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Atopic dermatitis (AD) is a multifactorial inflammatory skin disease resulting from interactions between genetic susceptibility and environmental factors. The pathogenesis of AD is poorly understood, and the treatment of recalcitrant AD is still challenging. There is accumulating evidence for new gene polymorphisms related to the epidermal barrier function and innate and adaptive immunity in patients with AD. Newly-found T cells and dendritic cell subsets, cytokines, chemokines and signaling pathways have extended our understanding of the molecular pathomechanism underlying AD. Genetic changes caused by environmental factors have been shown to contribute to the pathogenesis of AD. We herein present a review of the genetics, epigenetics, barrier dysfunction and immunological abnormalities in AD with a focus on updated molecular biology.

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Section: Geneticsmentioning

confidence: 99%

Molecular Mechanisms of Cutaneous Inflammatory Disorder: Atopic Dermatitis

Kim

Cho

et al. 2016

IJMS

106

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“…A recent finding among a Han Chinese population showed that polymorphisms in the high affinity receptor of IgE are associated with atopic dermatitis but not with urticaria, indicating that these diseases may have different genetic aetiologies, at least in respect to certain genetic polymorphisms [24]. …”

Section: Discussionmentioning

confidence: 99%

Urticaria in Monozygotic and Dizygotic Twins

et al. 2012

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Aim. To identify risk factors for urticaria, to determine the relative proportion of the susceptibility to urticaria that is due to genetic factors in an adult clinical twin sample, and to further determine whether the genetic susceptibility to urticaria overlaps with the genetic susceptibility to atopic diseases. Methods. A total of 256 complete twin pairs and 63 single twins, who were selected from sibships with self-reported asthma via a questionnaire survey of 21,162 adult twins from the Danish Twin Registry, were clinically interviewed about a history of urticaria and examined for atopic diseases. Data were analysed with Cox proportional hazards regression and variance components models. Results. A total of 151 individuals (26%) had a history of urticaria, whereas 24 (4%) had had symptoms within the past year. Female sex, HR = 2.09 (1.46–2.99), P = 0.000; hay fever, HR = 1.92 (1.36–2.72), P = 0.000; and atopic dermatitis, HR = 1.44 (1.02–2.06), P = 0.041 were significant risk factors for urticaria. After adjustment for sex and age at onset of urticaria in the index twin, the risk of urticaria was increased in MZ cotwins relative to DZ cotwins, HR = 1.42 (0.63–3.18), P = 0.394. Genetic factors explained 45% (16–74%), P = 0.005, of the variation in susceptibility to urticaria. The genetic correlation between urticaria and hay fever was 0.45 (0.01–0.89), P = 0.040. Conclusions. Susceptibility to urticaria is partly determined by genetic factors. Urticaria is more common in women, and in subjects with hay fever and atopic dermatitis, and shares genetic variance with hay fever.

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“…SNPs in the promoter region of the gene encoding the IgEbinding alpha-chain 8 (À344C>T and À95 T>C) have been associated with AD and/or high total IgE serum levels (80)(81)(82)(83)(84). The assumption that, besides cytokine genes mentioned earlier, the FCERIA gene plays a major role in the IgE response and allergic sensitization is further supported by a large and replicated genome-wide association study (GWAS) (76,85).…”

Section: Alpha-chain (Fceria)mentioning

confidence: 92%

Atopic dermatitis 2.0: from the clinical phenotype to the molecular taxonomy and stratified medicine

Bieber

2012

Allergy

165

125

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Atopic dermatitis (AD) is a paradigmatic inflammatory chronic skin disease. As for other chronic skin diseases, (i) the spectrum of the clinical phenotype and severity as well as (ii) the genetic background and (iii) the underlying mechanisms strongly suggest a high degree of pathophysiological heterogeneity yet leading to a similar clinical pattern, that is, the eczematous skin lesion, but showing distinct progression patterns. This review suggests to exploit the recent knowledge about AD for a novel approach proposing a tentative first molecular taxonomy of this disease based on the genotype and endophenotype. The consequences in terms of personalized prevention and management are delineated.As an evolution of the biomedical research and our genetic and pathophysiological understanding of complex diseases, we are currently experiencing a new trend in the classification of diseases moving from the purely phenotypic definition to a molecular taxonomy. It is expected that in future medicine, every disease will be characterized by three main groups of information: (i) the genotype, including epigenotypic information, (ii) the endophenotype (1) that comprises all available biomarkers (BMs), and (iii) the clinical phenotype (Fig. 1). Among all chronic inflammatory diseases, atopic dermatitis (AD) represents a paradigmatic condition because of its genetic and pathophysiological complexity (2) and finally the result thereof: the wide spectrum of clinical phenotype (3). This wide spectrum includes at one end the very minor forms such as atopic stigmata or simply dry skin with minimal itching and the erythrodermic and most severe form of AD at the other end. Due to the recent progress in the research of genetic, immunologic, and environmental factors (the so-called exposome) leading to AD, we are just starting to understand the complexity of the mechanisms underlying the variety in the clinical phenotype and to make first attempts to link the genotype and endophenotype to distinct clinical forms and courses of this disease such as the atopic march. After exposing a brief update of the clinical phenotype and pathophysiological aspects, this review introduces the concept of molecular taxonomy for AD and the consequences for its future management in the context of stratified or personalized medicine.

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Association of polymorphisms in the promoter region of FCER1A gene with atopic dermatitis, chronic uticaria, asthma, and serum immunoglobulin E levels in a Han Chinese population

Cited by 21 publications

References 25 publications

Molecular Mechanisms of Cutaneous Inflammatory Disorder: Atopic Dermatitis

Molecular Mechanisms of Cutaneous Inflammatory Disorder: Atopic Dermatitis

Urticaria in Monozygotic and Dizygotic Twins

Atopic dermatitis 2.0: from the clinical phenotype to the molecular taxonomy and stratified medicine

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