Original Articles: Mechanisms of AllergyIncreased total serum IgE levels in patients with asthma and promoter polymorphisms at CTLA4 and FCER1B☆
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rhPLD2 inhibits airway inflammation in an asthmatic murine model through induction of stable CD25 <sup>+</sup> Foxp3 <sup>+</sup> Tregs
2018, Molecular ImmunologyCitation Excerpt :These results suggest that rhPLD2 specifically suppresses airway eosinophil infiltration (Fig. 2A). Atopic allergies, including atopic (allergic) asthma and atopic dermatitis, are characterized by increased local and systemic production of IgE which can mediate AHR (Amit et al., 2014; Hizawa et al., 2001). The high IgE production is the result of high Th2 polarization in T cell responses.
Association of three sets of high-affinity IgE receptor (FcepsilonR1) polymorphisms with aspirin-intolerant asthma
2008, Respiratory MedicineCitation Excerpt :Although, we identified significant associations between the FCER1A-95T>C polymorphism and serum IgE specific for SEA and TSST-1, further studies using a larger sample size are necessary to confirm these associations. Previous population studies have reported significant associations between the MS4A2 polymorphism and total serum IgE levels in asthmatic patients.27,28 However, our results suggest that this is not the case for AIA patients.
Allergen-Specific IgG1 Provides Parsimonious Heritability Estimates for Atopy-Associated Immune Responses to Allergens
2007, Human ImmunologyCitation Excerpt :Recent evidence suggests that single nucleotide polymorphisms (SNPs) in the promoter regions of immune regulatory genes can profoundly impact upon the specific details of an immune response to allergens [36]. Three specific examples include SNPs in the CD14 endotoxin receptor gene that influences both allergen-specific IgE and IgG1 production among those with atopy [37], SNPs in the promoter region for inducible cofactor of stimulation that mediates T cell–B cell interaction during humoral response development [38], and CTLA-4 gene promoter SNPs that also impacts upon T cell–B cell interaction [39, 40]. Given that each of these gene promoter elements can have at least one of three genotypes (e.g., C/C, C/T, or T/T for the CD14 promoter), then there are at least 3 × 3 × 3 = 27 possible combinations taking all three together.
Stress and allergic diseases
2007, Psychoneuroimmunology, Two-Volume SetCluster Analysis Identifies 3 Phenotypes within Allergic Asthma
2018, Journal of Allergy and Clinical Immunology: In PracticeCitation Excerpt :Thus, although in both clusters IgE is a key etiopathogenic factor, as evident by positive specific IgE or skin prick testing and symptoms on exposure to the allergen, it is tempting to speculate that in cluster 1 the effect of environmental influences could be more evident than that of genetic influences, whereas in cluster 2 it could be the other way around. In this sense, associations between total serum IgE and polymorphisms of different genes have been described.23-25 This could be reflected in the higher levels of total serum IgE observed in cluster 2, in which genetic influences are purportedly stronger.
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Supported in part by a Grant-in-Aid for Scientific Research (10307013 and 11670559) from the Japanese Ministry of Education, Science, Sports and Culture.