Immunoglobulin constant heavy G chain genes as risk factors in childhood allergies (original) (raw)
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Genomics, 1997
served evidence for linkage of both asthma and ele-Linkage of asthma and high total serum IgE levels to vated total IgE concentrations to markers on chromochromosome 12q15-q24.1 has been recently described. some 12q15-q24.1 in an Afro-Caribbean population; To evaluate this region further in regard to total IgE evidence for linkage of log[total IgE] and elevated IgE responsiveness, we genotyped 52 unrelated German levels was also described in an inbred Caucasian popuchildren with persistently ''high'' total serum IgE (selation (1). The statistical approaches in this study were lected from a noninterventional prospective multicenthe transmission/disequilibrium test (TDT), affected ter cohort study) and their parents. We carefully desib-pair analysis, and multipoint analysis. Two gefined a most extreme IgE phenotype and analyzed it nome-wide searches on asthma and asthma-associated as a dichotomous trait. We tested for linkage between traits have been published (5, 6). Using multipoint high total IgE concentrations and nine polymorphic analysis in affected sib-pairs of different racial backmicrosatellite markers on chromosome 12q15-q24.1 grounds, chromosome 12q was one region that showed using the transmission/disequilibrium test. Evidence evidence for linkage to asthma in Caucasian and Hisfor linkage and allelic association for high total IgE panic sib-pairs in the Collaborative Study on the Gewas observed for four markers in this region. This
Allergen-specific IgE and IgG4 patterns among patients with different allergic diseases
World Allergy Organization Journal, 2018
Background: In addition to allergen-specific IgE (sIgE), allergen-specific IgG4 (sIgG4) antibodies are also involved in the immune response resulting from an allergen exposure. The aim of our study was to analyze sIgE and sIgG4 patterns in the most common allergic disorders: bronchial asthma, upper airway disorders and atopic dermatitis. Methods: In this study a screening analysis of blood serum samples from 673 patients aged from 6 months to 17 years with different allergic entities was performed on microarrays. sIgE and sIgG4 levels to the most common allergens were estimated. Results: sIgE response to most pollen allergens is more strongly associated with respiratory diseases than with atopic dermatitis, while sIgE responses to cat and dog dander are more strongly associated with bronchial asthma than with atopic dermatitis and upper airway disorders such as rhinosinusitis and allergic rhinitis. A lower prevalence of sIgG4 to pollen allergens in cases of atopic dermatitis is observed compared with that in cases of asthma and upper airway disorders. Analyzing all the allergic disorders, one can see that sIgG4 response to inhalant allergens is strongly associated with sensitization to the corresponding allergen. Conclusion: Allergen-specific IgE and IgG4 patterns that are relevant to concrete allergic diseases differ by sIgE and sIgG4 prevalences to defined allergens.
Journal of Allergy and Clinical Immunology, 1998
Study on the Genetics of Asthma (CSGA), which showed evidence for linkage in some regions, including chromosomes 5q31-q33 and 11q13 in African American families. Objectives: To clarify relative contributions of these regions to atopy in the same African American population, we have conducted further genetic linkage studies of specific IgE responses toward common inhaled allergens. Methods: We studied 328 individuals in 58 African American families participating in the CSGA. Specific IgE responses toward Dermatophagoides farinae, cat, dog, American cockroach, rye grass, and Bermuda grass, as measured by skin tests, were used for multipoint linkage analysis with polymorphic markers on chromosomes 5q31-q33 and 11q13. Results: Specific IgE response toward American cockroach showed evidence for linkage to chromosomes 5q31-q33 (P = .0050) and 11q13 (P = .017). Specific IgE response toward dog showed evidence for linkage with chromosome 5q31-q33 (P = .0043). Evidence for linkage with chromosome 11q13 was obtained for specific IgE responses toward Dermatophagoides farinae (P = .012), cat (P = .035), and Bermuda grass (P = .017). The presence of a positive ST response for at least 1 of 30 common allergens showed evidence for linkage to chromosomes 5q31-q33 (P = .017) and 11q13 (P = .00058).
Maternal Serum IgE, Cord Blood IgE, and Children’s Allergy: A Narrative Review
Journal of Pediatrics Review
Context: Asthma is chronic inflammatory disorder of the respiratory system in childhood. IgE has an important role in allergic disorders such as asthma. The aim of this study is to review the association between maternal serum IgE and incidence of childhood asthma. Evidence Acquisition: Three researchers searched all articles in PubMed, Scopus, Google and Embase databases related to maternal serum IgE, cord blood IgE, childhood asthma and incidence using key words such as maternal IgE, cord blood IgE, relation, association, childhood asthma, child allergy. Results: We found a few related articles on the topic of maternal IgE, cord blood IgE, and childhood asthma. We reviewed 11 articles for this study. Parental atopy and allergy are more important predictive factors for children's allergies such as asthma. IgE levels was higher in children whose mothers had higher IgE levels. Total IgE level was significantly higher in boys compared to girls. Conclusions: Increasing maternal and cord blood IgE may be a predictive factor for development of children asthma. More data is needed to clearify this relation.
Association between Gm allotypes and asthma severity from childhood to young middle age
Respiratory Medicine, 2008
Immunoglobulin constant heavy G chain (IGHG) gene polymorphisms are associated with atopy and can be determined by the serum Gm allotypes. We studied whether certain polymorphisms are related to asthma severity and to the extent or intensity of allergic sensitization in asthmatic subjects followed from childhood to young middle age. Fifty-five subjects (28 males) with childhood asthma were all followed-up prospectively on six occasions from a mean age of 9 to 35 years in a study including asthma severity scoring, spirometry, skin prick, and specific serum IgE antibody testing. At the last visit, extended lung function tests and a cold air challenge were performed, and IGHG gene polymorphisms were identified by the alternative serum IgG subclass allotypes, employing ELISA and double immunodiffusion. The 19 subjects with the homozygous IGHG*bf/*bf genotype (originating from the IGHG3*b and the IGHG1*f alleles, which are in strong linkage disequilibrium), showed significantly higher asthma scores, lower airway function, and greater bronchodilator responses from childhood to adulthood, and in middle age greater airway hyperresponsiveness, compared to the subjects with the IGHG*bf/*ga or IGHG*ga/*ga genotypes. Among the subjects sensitized to animal danders, those with the IGHG*bf/*bf genotype showed the highest specific IgE levels.
Linkage of High-Affinity Ige Receptor Gene with Bronchial Hyperreactivity, Even in Absence of Atopy
Lancet, 1995
Asthma is a manifestation of bronchial hyperreactivity (BHR) and forms part of the spectrum of atopic disease. Some pedigree studies of atopy have suggested linkage with the high-affinity IgE receptor (Fc epsilon RI beta) gene on chromosome 11q13, but others find no linkage. The molecular genetics of asthma and BHR have not been studied in the general population. We examined the genetic linkage of the Fc epsilon RI beta gene with clinical asthma and the underlying phenotypes of BHR (to methacholine) and atopy (defined by skinprick testing) in 123 affected sibling-pairs recruited from the general population. We found evidence of significant linkage of a highly polymorphic microsatellite marker in the fifth intron of the Fc epsilon RI beta gene to a diagnosis of asthma (18.0% excess of shared alleles, p = 0.002) and to BHR (21.7% excess of shared alleles, p = 0.001). Significant linkage was also observed in siblings sharing BHR when those with atopy were excluded (32.8% excess of shared alleles, p = 0.004). Atopy in the absence of BHR did not show significant linkage to the Fc epsilon RI beta gene (7.2% excess of shared alleles, p = 0.124). These findings suggest that mutations in the Fc epsilon RI beta gene or a closely linked gene influence the BHR underlying asthma, even in the absence of atopy.