TY - JOUR
T1 - Resolving the etiology of atopic disorders by using genetic analysis of racial ancestry
AU - Gupta, Jayanta
AU - Johansson, Elisabet
AU - Bernstein, Jonathan A.
AU - Chakraborty, Ranajit
AU - Khurana Hershey, Gurjit K.
AU - Rothenberg, Marc E.
AU - Mersha, Tesfaye B.
N1 - Funding Information:
Supported by National Institutes of Health grants K01 HL103165 , U19 AI066738 , U19 AI070235 , R01 DK076893 , R01 HL132344, and R37 A1045898 and the Diversity and Health Disparities Award of the Cincinnati Children's Research Foundation.
Publisher Copyright:
© 2016 American Academy of Allergy, Asthma & Immunology
PY - 2016/9/1
Y1 - 2016/9/1
N2 - Atopic dermatitis (AD), food allergy, allergic rhinitis, and asthma are common atopic disorders of complex etiology. The frequently observed atopic march from early AD to asthma, allergic rhinitis, or both later in life and the extensive comorbidity of atopic disorders suggest common causal mechanisms in addition to distinct ones. Indeed, both disease-specific and shared genomic regions exist for atopic disorders. Their prevalence also varies among races; for example, AD and asthma have a higher prevalence in African Americans when compared with European Americans. Whether this disparity stems from true genetic or race-specific environmental risk factors or both is unknown. Thus far, the majority of the genetic studies on atopic diseases have used populations of European ancestry, limiting their generalizability. Large-cohort initiatives and new analytic methods, such as admixture mapping, are currently being used to address this knowledge gap. Here we discuss the unique and shared genetic risk factors for atopic disorders in the context of ancestry variations and the promise of high-throughput “-omics”–based systems biology approach in providing greater insight to deconstruct their genetic and nongenetic etiologies. Future research will also focus on deep phenotyping and genotyping of diverse racial ancestry, gene-environment, and gene-gene interactions.
AB - Atopic dermatitis (AD), food allergy, allergic rhinitis, and asthma are common atopic disorders of complex etiology. The frequently observed atopic march from early AD to asthma, allergic rhinitis, or both later in life and the extensive comorbidity of atopic disorders suggest common causal mechanisms in addition to distinct ones. Indeed, both disease-specific and shared genomic regions exist for atopic disorders. Their prevalence also varies among races; for example, AD and asthma have a higher prevalence in African Americans when compared with European Americans. Whether this disparity stems from true genetic or race-specific environmental risk factors or both is unknown. Thus far, the majority of the genetic studies on atopic diseases have used populations of European ancestry, limiting their generalizability. Large-cohort initiatives and new analytic methods, such as admixture mapping, are currently being used to address this knowledge gap. Here we discuss the unique and shared genetic risk factors for atopic disorders in the context of ancestry variations and the promise of high-throughput “-omics”–based systems biology approach in providing greater insight to deconstruct their genetic and nongenetic etiologies. Future research will also focus on deep phenotyping and genotyping of diverse racial ancestry, gene-environment, and gene-gene interactions.
KW - -omics
KW - Atopic march
KW - admixture mapping
KW - allergic rhinitis
KW - asthma
KW - atopic dermatitis
KW - food allergy
KW - gene-environment interaction
KW - phenotyping
KW - racial ancestry
UR - http://www.scopus.com/inward/record.url?scp=84995487877&partnerID=8YFLogxK
U2 - 10.1016/j.jaci.2016.02.045
DO - 10.1016/j.jaci.2016.02.045
M3 - Review article
C2 - 27297995
AN - SCOPUS:84995487877
SN - 0091-6749
VL - 138
SP - 676
EP - 699
JO - The Journal of Allergy and Clinical Immunology
JF - The Journal of Allergy and Clinical Immunology
IS - 3
ER -