ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Demethylation of the human eotaxin-3 gene promoter leads to the elevated expression of eotaxin-3.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Twin and family studies reveal strong environmental and weaker genetic cues explaining heritability of eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2014Trial
- Unravelling the pathogenesis of Eosinophilic Esophagitis from genetic predisposition to environmental triggers.Clinical and experimental immunology · 2025Review
- Common and disparate clinical presentations and mechanisms in different eosinophilic gastrointestinal diseases.The Journal of allergy and clinical immunology · 2024Review
- Expression profiling identifies key genes and biological functions associated with eosinophilic esophagitis in human patients.Frontiers in allergy · 2023Article
- Role of genetics, environment, and their interactions in the pathogenesis of eosinophilic esophagitis.Current opinion in immunology · 2019Review
- Epithelial origin of eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2018Review
- 8-Oxoguanine DNA glycosylase 1: Beyond repair of the oxidatively modified base lesions.Redox biology · 2018Review
- Forkhead box protein 3 demethylation is associated with tolerance induction in peanut-induced intestinal allergy.The Journal of allergy and clinical immunology · 2018Article
- Synaptopodin is upregulated by IL-13 in eosinophilic esophagitis and regulates esophageal epithelial cell motility and barrier integrity.JCI insight · 2017Article
- Procyanidin A2 Modulates IL-4-Induced CCL26 Production in Human Alveolar Epithelial Cells.International journal of molecular sciences · 2016Article
- Mechanisms of Disease of Eosinophilic Esophagitis.Annual review of pathology · 2016Review
- Eosinophilic Esophagitis: A Comprehensive Review.Clinical reviews in allergy & immunology · 2016Review
- The Immunologic Mechanisms of Eosinophilic Esophagitis.Current allergy and asthma reports · 2016Review
- Neurotrophic tyrosine kinase receptor 1 is a direct transcriptional and epigenetic target of IL-13 involved in allergic inflammation.Mucosal immunology · 2015Article
- Translating new developments in eosinophilic esophagitis pathogenesis into clinical practice.Current treatment options in gastroenterology · 2015Article
- Genetic and epigenetic underpinnings of eosinophilic esophagitis.Gastroenterology clinics of North America · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA demethylation has been primarily studied in the context of development biology, cell fate, and cancer, with less attention on inflammation. In this article, we investigate the association between DNA methylation and production of the chemoattractant cytokine eotaxin-3 in the tissue of patients with allergic disease. Regions of the human eotaxin-3 promoter were found to be hypomethylated in primary epithelial cells obtained from allergic tissue compared with normal control tissue. The demethylation of a specific CpG site (designated CpG 2), which is juxtaposed to a key cAMP-responsive element site, was significantly demethylated in patient-derived compared with normal control tissue-derived epithelial cells. Levels of methylation at CpG 2 inversely correlated with basal and IL-13-induced eotaxin-3 gene expression. Conversely, global inhibition of methylation with 5-azacytidine promoted eotaxin-3 production in association with decreasing CpG 2 methylation. In addition, the basal and IL-13-induced eotaxin-3 transcriptional activity was suppressed by promoter methylation using a methylation-free in vitro system. Furthermore, EMSAs demonstrated that the attachment of CREB binding protein and activating transcription factor 2 (ATF-2) to the cAMP-responsive element site was methylation dependent. Taken together, these data identify a contributory role for DNA methylation in regulating eotaxin-3 production in human allergic inflammation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.