Genetic variability of the high-affinity IgE receptor α-subunit (FcεRIα)

Potaczek, Daniel P.; Nishiyama, Chiharu; Sanak, Marek; Szczeklik, A; Okumura, Ko

doi:10.1007/s12026-008-8042-0

Cited by 18 publications

(9 citation statements)

References 41 publications

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“…While increased IgE levels are protective against infection and reinfection, elevated IgG4 levels increase predisposition to infection and reinfection. Recent studies have found strong association between IgE levels and certain loci in the human genome, including: the cytokine gene cluster on chromosome 5q31-q33 (SM1), which also controls infection with schistosomiasis [7], [64]–[67]; FCER1A on chromosome 1q23, which is the gene encoding the alpha chain of the high affinity receptor for IgE [11], [14]; STAT4 on chromosome 2q32 [12], [64] which controls Th1 development; STAT6 on chromosome 12q13 [12], [13], [15], [64] and GATA3 on chromosome 10p15 [12], [64] which control Th2 development; and the Th2 cytokine receptor cluster in 16p12 region of the human genome [7], [64]. We had expected to identify studies assessing association between reinfection and several immunogenetic factors including variations in these loci; however, there were few or no studies on the host immunogenetic factors of reinfection with schistosomes, an important theme for further research.…”

Section: Discussionmentioning

confidence: 99%

Host Determinants of Reinfection with Schistosomes in Humans: A Systematic Review and Meta-analysis

et al. 2014

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BackgroundSchistosomiasis is still a major public health burden in the tropics and subtropics. Although there is an effective chemotherapy (Praziquantel) for this disease, reinfection occurs rapidly after mass drug administration (MDA). Because the entire population do not get reinfected at the same rate, it is possible that host factors may play a dominant role in determining resistance or susceptibility to reinfection with schistosomes. Here, we systematically reviewed and meta-analyzed studies that reported associations between reinfection with the principal human-infecting species (S. mansoni, S. japonicum and S. haematobium) and host socio-demographic, epidemiological, immunological and genetic factors.Methodology/Principal FindingsPubMed, Scopus, Google Scholar, Cochrane Review Library and African Journals Online public databases were searched in October 2013 to retrieve studies assessing association of host factors with reinfection with schistosomes. Meta-analysis was performed to generate pooled odds ratios and standardized mean differences as overall effect estimates for dichotomous and continuous variables, respectively. Quality assessment of included studies, heterogeneity between studies and publication bias were also assessed. Out of the initial 2739 records, 109 studies were included in the analyses, of which only 32 studies with 37 data sets were eligible for quantitative data synthesis. Among several host factors identified, strong positive association was found with age and pre-treatment intensity, and only slightly for gender. These factors are major determinants of exposure and disease transmission. Significant positive association was found with anti-SWA IgG4 level, and a negative overall effect for association with IgE levels. This reconfirmed the concept that IgE/IgG4 balance is a major determinant of protective immunity against schistosomiasis. Other identified determinants were reported by a small number of studies to enable interpretation.ConclusionsOur data contribute to the understanding of host-parasite interaction as it affects reinfection, and is a potential tool to guide planning and tailoring of community interventions to target high-risk groups.

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Section: Discussionmentioning

confidence: 99%

Host Determinants of Reinfection with Schistosomes in Humans: A Systematic Review and Meta-analysis

et al. 2014

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“…[72][73][74] Genes that have been extensively replicated include the beta2 adrenergic receptor gene, [75][76][77] as well as genes involving cytokines, receptors, signaling proteins, and transcription factors involved in Th1 and Th2 cell differentiation, such as IL4, IL4RA, IFNG, IFNGR1, STAT6, GATA3, and TBX21, [78][79][80][81][82][83][84][85] as well as genes involved in the cellular responses that characterize atopic disease, such as IL13 and its receptor and the FCER1B gene. [86][87][88][89][90] Over the past decade, genomewide association studies (GWASs) have been used extensively to investigate the genetic bases of common complex diseases, including asthma. 91,92 Before GWAS, many candidate gene studies were performed for asthma susceptibility 93,94 ; however, most of the positive associations were not replicated in GWASs, because of differences in either phenotype definition or the populations studied (either in terms of ancestry or environmental exposures), or because of false positives.…”

Section: Genetics Of Asthmamentioning

confidence: 99%

Asthma risk factors

Toskala

Kennedy

2015

Int Forum Allergy Rhinol

174

122

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Asthma represents a dysfunctional interaction with our genes and the environment to which they are exposed, especially in fetal and early infant life. The increasing prevalence of asthma in all age groups indicate that our living environment and immunity are in imbalance with each other reacting with airway inflammation to the environmental exposures and often non-harmful proteins, such as allergens causing the current "asthma and allergy epidemic." Because of the close relationship between asthma and chronic rhinosinusitis, it is important that otolaryngologists have a good understanding of asthma, the etiologic factors associated with disease, and its evaluation and management.

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“…Alternatively, genetically determined higher FceRI(a) expression on bashophils and/or mast cells may enhance IgE-FceRI(a)-mediated allergen-induced activation of those cells [187,188]. In turn, increased secretion of IL-4 and IL-13 [189][190][191][192] and expression of CD40L [191,193] by bashophils and/or mast cells could stimulate further B cells to switch towards IgE production [1,194].…”

Section: Chromosome 1q23 Fcer1amentioning

confidence: 99%

Current concepts of IgE regulation and impact of genetic determinants

Potaczek

Kabesch

2012

Clin Experimental Allergy

100

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Immunoglobulin E (IgE) mediated immune responses seem to be directed against parasites and neoplasms, but are best known for their involvement in allergies. The IgE network is tightly controlled at different levels as outlined in this review. Genetic determinants were suspected to influence IgE regulation and IgE levels considerably for many years. Linkage and candidate gene studies suggested a number of loci and genes to correlate with total serum IgE levels, and recently genome-wide association studies (GWAS) provided the power to identify genetic determinants for total serum IgE levels: 1q23 (FCER1A), 5q31 (RAD50, IL13, IL4), 12q13 (STAT6), 6p21.3 (HLA-DRB1) and 16p12 (IL4R, IL21R). In this review, we analyse the potential role of these GWAS hits in the IgE network and suggest mechanisms of how genes and genetic variants in these loci may influence IgE regulation.

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Genetic variability of the high-affinity IgE receptor α-subunit (FcεRIα)

Cited by 18 publications

References 41 publications

Host Determinants of Reinfection with Schistosomes in Humans: A Systematic Review and Meta-analysis

Host Determinants of Reinfection with Schistosomes in Humans: A Systematic Review and Meta-analysis

Asthma risk factors

Current concepts of IgE regulation and impact of genetic determinants

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