A genome-wide association study of plasma total IgE concentrations in the Framingham Heart Study
Atopy and plasma IgE concentration are genetically complex traits, and the specific genetic risk factors that lead to IgE dysregulation and clinical atopy are an area of active investigation. We sought to ascertain the genetic risk factors that lead to IgE dysregulation. A genome-wide association st...
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| Vydáno v: | Journal of allergy and clinical immunology Ročník 129; číslo 3; s. 840 - 845.e21 |
|---|---|
| Hlavní autoři: | , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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New York, NY
Mosby, Inc
01.03.2012
Elsevier Elsevier Limited |
| Témata: | |
| ISSN: | 0091-6749, 1097-6825, 1097-6825 |
| On-line přístup: | Získat plný text |
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| Abstract | Atopy and plasma IgE concentration are genetically complex traits, and the specific genetic risk factors that lead to IgE dysregulation and clinical atopy are an area of active investigation.
We sought to ascertain the genetic risk factors that lead to IgE dysregulation.
A genome-wide association study (GWAS) was performed in 6819 participants from the Framingham Heart Study (FHS). Seventy of the top single nucleotide polymorphisms (SNPs) were selected based on P values and linkage disequilibrium among neighboring SNPs and evaluated in a meta-analysis with 5 independent populations from the Cooperative Health Research in the Region of Augsburg cohort, the British 1958 Birth Cohort, and the Childhood Asthma Management Program cohort.
Thirteen SNPs located in the region of 3 genes, FCER1A, signal transducer and activator of transcription 6 (STAT6), and IL13, were found to have genome-wide significance in the FHS cohort GWAS. The most significant SNPs from the 3 regions were rs2251746 (FCER1A, P = 2.11 × 10−12), rs1059513 (STAT6, P = 2.87 × 10−8), and rs1295686 (IL13, P = 3.55 × 10−8). Four additional gene regions, HLA-G, HLA-DQA2, HLA-A, and Duffy blood group, chemokine receptor (DARC), reached genome-wide statistical significance in a meta-analysis combining the FHS and replication cohorts, although the DARC association did not appear independent of SNPs in the nearby FCER1A gene.
This GWAS of the FHS cohort has identified genetic loci in HLA genes that might have a role in the pathogenesis of IgE dysregulation and atopy. It also confirmed the association of the known susceptibility loci FCER1A, STAT6, and IL13 for the dysregulation of total IgE. |
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| AbstractList | Atopy and plasma IgE concentration are genetically complex traits, and the specific genetic risk factors that lead to IgE dysregulation and clinical atopy are an area of active investigation.
We sought to ascertain the genetic risk factors that lead to IgE dysregulation.
A genome-wide association study (GWAS) was performed in 6819 participants from the Framingham Heart Study (FHS). Seventy of the top single nucleotide polymorphisms (SNPs) were selected based on P values and linkage disequilibrium among neighboring SNPs and evaluated in a meta-analysis with 5 independent populations from the Cooperative Health Research in the Region of Augsburg cohort, the British 1958 Birth Cohort, and the Childhood Asthma Management Program cohort.
Thirteen SNPs located in the region of 3 genes, FCER1A, signal transducer and activator of transcription 6 (STAT6), and IL13, were found to have genome-wide significance in the FHS cohort GWAS. The most significant SNPs from the 3 regions were rs2251746 (FCER1A, P = 2.11 × 10−12), rs1059513 (STAT6, P = 2.87 × 10−8), and rs1295686 (IL13, P = 3.55 × 10−8). Four additional gene regions, HLA-G, HLA-DQA2, HLA-A, and Duffy blood group, chemokine receptor (DARC), reached genome-wide statistical significance in a meta-analysis combining the FHS and replication cohorts, although the DARC association did not appear independent of SNPs in the nearby FCER1A gene.
This GWAS of the FHS cohort has identified genetic loci in HLA genes that might have a role in the pathogenesis of IgE dysregulation and atopy. It also confirmed the association of the known susceptibility loci FCER1A, STAT6, and IL13 for the dysregulation of total IgE. BACKGROUND: Atopy and plasma IgE concentration are genetically complex traits, and the specific genetic risk factors that lead to IgE dysregulation and clinical atopy are an area of active investigation. OBJECTIVE: We sought to ascertain the genetic risk factors that lead to IgE dysregulation. METHODS: A genome-wide association study (GWAS) was performed in 6819 participants from the Framingham Heart Study (FHS). Seventy of the top single nucleotide polymorphisms (SNPs) were selected based on P values and linkage disequilibrium among neighboring SNPs and evaluated in a meta-analysis with 5 independent populations from the Cooperative Health Research in the Region of Augsburg cohort, the British 1958 Birth Cohort, and the Childhood Asthma Management Program cohort. RESULTS: Thirteen SNPs located in the region of 3 genes, FCER1A, signal transducer and activator of transcription 6 (STAT6), and IL13, were found to have genome-wide significance in the FHS cohort GWAS. The most significant SNPs from the 3 regions were rs2251746 (FCER1A, P = 2.11 × 10⁻¹²), rs1059513 (STAT6, P = 2.87 × 10⁻⁸), and rs1295686 (IL13, P = 3.55 × 10⁻⁸). Four additional gene regions, HLA-G, HLA-DQA2, HLA-A, and Duffy blood group, chemokine receptor (DARC), reached genome-wide statistical significance in a meta-analysis combining the FHS and replication cohorts, although the DARC association did not appear independent of SNPs in the nearby FCER1A gene. CONCLUSION: This GWAS of the FHS cohort has identified genetic loci in HLA genes that might have a role in the pathogenesis of IgE dysregulation and atopy. It also confirmed the association of the known susceptibility loci FCER1A, STAT6, and IL13 for the dysregulation of total IgE. Atopy and plasma IgE concentration are genetically complex traits, and the specific genetic risk factors that lead to IgE dysregulation and clinical atopy are an area of active investigation. We sought to ascertain the genetic risk factors that lead to IgE dysregulation. A genome-wide association study (GWAS) was performed in 6819 participants from the Framingham Heart Study (FHS). Seventy of the top single nucleotide polymorphisms (SNPs) were selected based on P values and linkage disequilibrium among neighboring SNPs and evaluated in a meta-analysis with 5 independent populations from the Cooperative Health Research in the Region of Augsburg cohort, the British 1958 Birth Cohort, and the Childhood Asthma Management Program cohort. Thirteen SNPs located in the region of 3 genes, FCER1A, signal transducer and activator of transcription 6 (STAT6), and IL13, were found to have genome-wide significance in the FHS cohort GWAS. The most significant SNPs from the 3 regions were rs2251746 (FCER1A, P = 2.11 × 10(-12)), rs1059513 (STAT6, P = 2.87 × 10(-8)), and rs1295686 (IL13, P = 3.55 × 10(-8)). Four additional gene regions, HLA-G, HLA-DQA2, HLA-A, and Duffy blood group, chemokine receptor (DARC), reached genome-wide statistical significance in a meta-analysis combining the FHS and replication cohorts, although the DARC association did not appear independent of SNPs in the nearby FCER1A gene. This GWAS of the FHS cohort has identified genetic loci in HLA genes that might have a role in the pathogenesis of IgE dysregulation and atopy. It also confirmed the association of the known susceptibility loci FCER1A, STAT6, and IL13 for the dysregulation of total IgE. Background: Atopy and plasma IgE concentration are genetically complex traits, and the specific genetic risk factors that lead to IgE dysregulation and clinical atopy are an area of active investigation. Objective: We sought to ascertain the genetic risk factors that lead to IgE dysregulation. Methods: A genome-wide association study (GWAS) was performed in 6819 participants from the Framingham Heart Study (FHS). Seventy of the top single nucleotide polymorphisms (SNPs) were selected based on P values and linkage disequilibrium among neighboring SNPs and evaluated in a meta-analysis with 5 independent populations from the Cooperative Health Research in the Region of Augsburg cohort, the British 1958 Birth Cohort, and the Childhood Asthma Management Program cohort. Results: Thirteen SNPs located in the region of 3 genes, FCER1A, signal transducer and activator of transcription 6 (STAT6), and IL13, were found to have genome-wide significance in the FHS cohort GWAS. The most significant SNPs from the 3 regions were rs2251746 (FCER1A, P = 2.11 10-12), rs1059513 (STAT6, P = 2.87 10-8), and rs1295686 (IL13, P = 3.55 10-8). Four additional gene regions, HLA-G, HLA-DQA2, HLA-A, and Duffy blood group, chemokine receptor (DARC), reached genome-wide statistical significance in a meta-analysis combining the FHS and replication cohorts, although the DARC association did not appear independent of SNPs in the nearby FCER1A gene. Conclusions: This GWAS of the FHS cohort has identified genetic loci in HLA genes that might have a role in the pathogenesis of IgE dysregulation and atopy. It also confirmed the association of the known susceptibility loci FCER1A, STAT6, and IL13 for the dysregulation of total IgE. Background Atopy and plasma IgE concentration are genetically complex traits, and the specific genetic risk factors that lead to IgE dysregulation and clinical atopy are an area of active investigation. Objective We sought to ascertain the genetic risk factors that lead to IgE dysregulation. Methods A genome-wide association study (GWAS) was performed in 6819 participants from the Framingham Heart Study (FHS). Seventy of the top single nucleotide polymorphisms (SNPs) were selected based onPvalues and linkage disequilibrium among neighboring SNPs and evaluated in a meta-analysis with 5 independent populations from the Cooperative Health Research in the Region of Augsburg cohort, the British 1958 Birth Cohort, and the Childhood Asthma Management Program cohort. Results Thirteen SNPs located in the region of 3 genes,FCER1A, signal transducer and activator of transcription 6(STAT6), andIL13, were found to have genome-wide significance in the FHS cohort GWAS. The most significant SNPs from the 3 regions were rs2251746 (FCER1A,P = 2.11 × 10-12), rs1059513 (STAT6,P = 2.87 × 10-8), and rs1295686 (IL13,P = 3.55 × 10-8). Four additional gene regions,HLA-G,HLA-DQA2,HLA-A, and Duffy blood group, chemokine receptor(DARC), reached genome-wide statistical significance in a meta-analysis combining the FHS and replication cohorts, although theDARCassociation did not appear independent of SNPs in the nearbyFCER1Agene. Conclusion This GWAS of the FHS cohort has identified genetic loci inHLAgenes that might have a role in the pathogenesis of IgE dysregulation and atopy. It also confirmed the association of the known susceptibility lociFCER1A,STAT6, andIL13for the dysregulation of total IgE. Background Atopy and plasma IgE concentration are genetically complex traits, and the specific genetic risk factors that lead to IgE dysregulation and clinical atopy are an area of active investigation. Objective We sought to ascertain the genetic risk factors that lead to IgE dysregulation. Methods A genome-wide association study (GWAS) was performed in 6819 participants from the Framingham Heart Study (FHS). Seventy of the top single nucleotide polymorphisms (SNPs) were selected based on P values and linkage disequilibrium among neighboring SNPs and evaluated in a meta-analysis with 5 independent populations from the Cooperative Health Research in the Region of Augsburg cohort, the British 1958 Birth Cohort, and the Childhood Asthma Management Program cohort. Results Thirteen SNPs located in the region of 3 genes, FCER1A , signal transducer and activator of transcription 6 (STAT6) , and IL13 , were found to have genome-wide significance in the FHS cohort GWAS. The most significant SNPs from the 3 regions were rs2251746 ( FCER1A , P = 2.11 × 10−12 ), rs1059513 ( STAT6 , P = 2.87 × 10−8 ), and rs1295686 ( IL13 , P = 3.55 × 10−8 ). Four additional gene regions, HLA-G , HLA-DQA2 , HLA-A , and Duffy blood group, chemokine receptor (DARC) , reached genome-wide statistical significance in a meta-analysis combining the FHS and replication cohorts, although the DARC association did not appear independent of SNPs in the nearby FCER1A gene. Conclusion This GWAS of the FHS cohort has identified genetic loci in HLA genes that might have a role in the pathogenesis of IgE dysregulation and atopy. It also confirmed the association of the known susceptibility loci FCER1A , STAT6 , and IL13 for the dysregulation of total IgE. Atopy and plasma IgE concentration are genetically complex traits, and the specific genetic risk factors that lead to IgE dysregulation and clinical atopy are an area of active investigation.BACKGROUNDAtopy and plasma IgE concentration are genetically complex traits, and the specific genetic risk factors that lead to IgE dysregulation and clinical atopy are an area of active investigation.We sought to ascertain the genetic risk factors that lead to IgE dysregulation.OBJECTIVEWe sought to ascertain the genetic risk factors that lead to IgE dysregulation.A genome-wide association study (GWAS) was performed in 6819 participants from the Framingham Heart Study (FHS). Seventy of the top single nucleotide polymorphisms (SNPs) were selected based on P values and linkage disequilibrium among neighboring SNPs and evaluated in a meta-analysis with 5 independent populations from the Cooperative Health Research in the Region of Augsburg cohort, the British 1958 Birth Cohort, and the Childhood Asthma Management Program cohort.METHODSA genome-wide association study (GWAS) was performed in 6819 participants from the Framingham Heart Study (FHS). Seventy of the top single nucleotide polymorphisms (SNPs) were selected based on P values and linkage disequilibrium among neighboring SNPs and evaluated in a meta-analysis with 5 independent populations from the Cooperative Health Research in the Region of Augsburg cohort, the British 1958 Birth Cohort, and the Childhood Asthma Management Program cohort.Thirteen SNPs located in the region of 3 genes, FCER1A, signal transducer and activator of transcription 6 (STAT6), and IL13, were found to have genome-wide significance in the FHS cohort GWAS. The most significant SNPs from the 3 regions were rs2251746 (FCER1A, P = 2.11 × 10(-12)), rs1059513 (STAT6, P = 2.87 × 10(-8)), and rs1295686 (IL13, P = 3.55 × 10(-8)). Four additional gene regions, HLA-G, HLA-DQA2, HLA-A, and Duffy blood group, chemokine receptor (DARC), reached genome-wide statistical significance in a meta-analysis combining the FHS and replication cohorts, although the DARC association did not appear independent of SNPs in the nearby FCER1A gene.RESULTSThirteen SNPs located in the region of 3 genes, FCER1A, signal transducer and activator of transcription 6 (STAT6), and IL13, were found to have genome-wide significance in the FHS cohort GWAS. The most significant SNPs from the 3 regions were rs2251746 (FCER1A, P = 2.11 × 10(-12)), rs1059513 (STAT6, P = 2.87 × 10(-8)), and rs1295686 (IL13, P = 3.55 × 10(-8)). Four additional gene regions, HLA-G, HLA-DQA2, HLA-A, and Duffy blood group, chemokine receptor (DARC), reached genome-wide statistical significance in a meta-analysis combining the FHS and replication cohorts, although the DARC association did not appear independent of SNPs in the nearby FCER1A gene.This GWAS of the FHS cohort has identified genetic loci in HLA genes that might have a role in the pathogenesis of IgE dysregulation and atopy. It also confirmed the association of the known susceptibility loci FCER1A, STAT6, and IL13 for the dysregulation of total IgE.CONCLUSIONThis GWAS of the FHS cohort has identified genetic loci in HLA genes that might have a role in the pathogenesis of IgE dysregulation and atopy. It also confirmed the association of the known susceptibility loci FCER1A, STAT6, and IL13 for the dysregulation of total IgE. |
| Author | Granada, Mark Himes, Blanca E. Cruikshank, William W. O'Connor, George T. Wilk, Jemma B. Hunninghake, Gary M. Farrer, Lindsay A. Heinrich, Joachim Celedón, Juan C. Center, David M. Albrecht, Eva Weiss, Scott T. Tuzova, Marina Strachan, David P. Weidinger, Stephan Gieger, Christian |
| Author_xml | – sequence: 1 givenname: Mark surname: Granada fullname: Granada, Mark organization: Pulmonary Center, Boston University School of Medicine, Boston, Mass – sequence: 2 givenname: Jemma B. surname: Wilk fullname: Wilk, Jemma B. organization: Division of Aging, Department of Medicine, Brigham and Women's Hospital, Boston, Mass – sequence: 3 givenname: Marina surname: Tuzova fullname: Tuzova, Marina organization: Pulmonary Center, Boston University School of Medicine, Boston, Mass – sequence: 4 givenname: David P. surname: Strachan fullname: Strachan, David P. organization: Division of Community Health Science, St George's, University of London, London, United Kingdom – sequence: 5 givenname: Stephan surname: Weidinger fullname: Weidinger, Stephan organization: Department of Dermatology, University of Kiel, Kiel, Germany – sequence: 6 givenname: Eva surname: Albrecht fullname: Albrecht, Eva organization: Institute of Genetic Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany – sequence: 7 givenname: Christian surname: Gieger fullname: Gieger, Christian organization: Institute of Genetic Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany – sequence: 8 givenname: Joachim surname: Heinrich fullname: Heinrich, Joachim organization: Institute of Epidemiology I, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany – sequence: 9 givenname: Blanca E. surname: Himes fullname: Himes, Blanca E. organization: Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, and the Department of Medicine, Harvard Medical School, Boston, Mass – sequence: 10 givenname: Gary M. surname: Hunninghake fullname: Hunninghake, Gary M. organization: Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, and the Department of Medicine, Harvard Medical School, Boston, Mass – sequence: 11 givenname: Juan C. surname: Celedón fullname: Celedón, Juan C. organization: Division of Pediatric Pulmonary Medicine, Allergy and Immunology, Children's Hospital of Pittsburgh of UPMC, University of Pittsburgh School of Medicine, Pittsburgh, Pa – sequence: 12 givenname: Scott T. surname: Weiss fullname: Weiss, Scott T. organization: Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, and the Department of Medicine, Harvard Medical School, Boston, Mass – sequence: 13 givenname: William W. surname: Cruikshank fullname: Cruikshank, William W. organization: Pulmonary Center, Boston University School of Medicine, Boston, Mass – sequence: 14 givenname: Lindsay A. surname: Farrer fullname: Farrer, Lindsay A. organization: Departments of Medicine, Neurology, Ophthalmology, and Genetics and Genomics, Boston University School of Medicine, and the Departments of Epidemiology and Biostatistics, Boston University School of Public Health, Boston, Mass – sequence: 15 givenname: David M. surname: Center fullname: Center, David M. organization: Pulmonary Center, Boston University School of Medicine, Boston, Mass – sequence: 16 givenname: George T. surname: O'Connor fullname: O'Connor, George T. email: goconnor@bu.edu organization: Pulmonary Center, Boston University School of Medicine, Boston, Mass |
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| ContentType | Journal Article |
| Copyright | 2011 American Academy of Allergy, Asthma & Immunology American Academy of Allergy, Asthma & Immunology 2015 INIST-CNRS Copyright © 2011 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved. Copyright Elsevier Limited Mar 2012 |
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| Keywords | B58C GWAS atopy asthma FHS KORA DARC CEU RAD50 SNP genome-wide association study LD Total IgE MACH STAT6 CAMP Linkage disequilibrium Signal transducer and activator of transcription 6 Markov Chain haplotyping Duffy blood group, chemokine receptor RAD50 homolog (Saccharomyces cerevisiae) Childhood Asthma Management Program Framingham Heart Study Western European British 1958 Birth Cohort Cooperative Health Research in the Region of Augsburg Single nucleotide polymorphism Heart Allergy Lung disease Immunopathology Respiratory disease IgE Concentration Asthma Atopy Blood plasma Association Immunology Bronchus disease Circulatory system Obstructive pulmonary disease Genome |
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| Snippet | Atopy and plasma IgE concentration are genetically complex traits, and the specific genetic risk factors that lead to IgE dysregulation and clinical atopy are... Background Atopy and plasma IgE concentration are genetically complex traits, and the specific genetic risk factors that lead to IgE dysregulation and clinical... BACKGROUND: Atopy and plasma IgE concentration are genetically complex traits, and the specific genetic risk factors that lead to IgE dysregulation and... Background: Atopy and plasma IgE concentration are genetically complex traits, and the specific genetic risk factors that lead to IgE dysregulation and... |
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| SubjectTerms | Adult Allergies Allergy and Immunology asthma atopy Biological and medical sciences blood groups Cardiovascular Diseases - blood Cardiovascular Diseases - epidemiology Cardiovascular Diseases - genetics Cardiovascular Diseases - immunology chemokine receptors childhood Chronic obstructive pulmonary disease, asthma Cohort Studies Female Fundamental and applied biological sciences. Psychology Fundamental immunology Genes Genetic Predisposition to Disease Genome-Wide Association Study heart HLA Antigens - genetics Humans Hypersensitivity - blood Hypersensitivity - epidemiology Hypersensitivity - genetics Hypersensitivity - immunology immunoglobulin E Immunoglobulin E - blood Immunopathology Interleukin-13 - genetics Linkage Disequilibrium loci Male Medical research Medical sciences meta-analysis Middle Aged pathogenesis Plasma Pneumology Polymorphism, Single Nucleotide Receptors, IgE - genetics Risk Factors Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis signal transduction single nucleotide polymorphism STAT6 Transcription Factor - genetics Studies Total IgE transcription factors United Kingdom United States |
| Title | A genome-wide association study of plasma total IgE concentrations in the Framingham Heart Study |
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