ArticleEuropean journal of human genetics : EJHG2009
STAT3 single-nucleotide polymorphisms and STAT3 mutations associated with hyper-IgE syndrome are not responsible for increased serum IgE serum levels in asthma families.
Article in European journal of human genetics : EJHG, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Rare clinical presentations of hyper-IgE syndrome in a patient with dental abnormalities: A case report.Clinical case reports · 2021Article
- The role of regulatory T cells and genes involved in their differentiation in pathogenesis of selected inflammatory and neoplastic skin diseases. Part III: Polymorphisms of genes involved in Tregs' activation and function.Postepy dermatologii i alergologii · 2017Review
- Immune-related gene polymorphisms in pulmonary diseases.Toxicology · 2017Review
- The Expression ofTanaffos · 2017Article
- Antibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis.Journal of leukocyte biology · 2016Article
- Insights into pathophysiology of dystropy through the analysis of gene networks: an example of bronchial asthma and tuberculosis.Immunogenetics · 2014Article
- Review
- An understanding of the genetic basis of asthma.The Indian journal of medical research · 2011Review
- Th17 cells, Job's syndrome and HIV: opportunities for bacterial and fungal infections.Current opinion in HIV and AIDS · 2010Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in STAT3 (signal transducer and activator of transcription 3) have recently been found to cause the hyper-IgE syndrome (HIES) - a rare immunodeficiency syndrome including complex somatic features. We now tested whether STAT3 mutations or single-nucleotide polymorphisms (SNPs) within STAT3 may be responsible for increased IgE levels in asthmatic children. We genotyped DNA samples from 918 individuals of 217 core families by MALDI-TOF mass spectrometry. SNPs were selected from previous reports, by functional relevance and haplotype-tagging capacity. In 24 assays, including the recently described HIES mutations, no variant was detected. In another 27 SNP assays, there was no association of any STAT3 variant with asthma, allergic rhinitis or eczema. In addition, neither total and specific IgE and eosinophil count nor any lung function parameter showed any significant association. When combining high eosinophil counts and high total IgE levels to an HIES-like trait, four SNPs in the 5'-UTR of STAT3 were slightly overtransmitted. A minor fraction of asthmatic children may possibly have an alternate STAT3 promoter architecture influencing joined IgE and eosinophil upregulation. While an overall effect of STAT3 mutations on serum IgE is unlikely in asthma children.
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