Immunological Reviews, July, 2011, Vol.242, p.10(21)
To authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1600-065X.2011.01029.x Byline: Carole Ober (1), Tsung-Chieh Yao (2) Keywords: association studies; linkage studies; genome-wide association studies; asthma; allergic disease; atopy Abstract: Summary: Asthma and allergy are common conditions with complex etiologies involving both genetic and environmental contributions. Recent genome-wide association studies (GWAS) and meta-analyses of GWAS have begun to shed light on both common and distinct pathways that contribute to asthma and allergic diseases. Associations with variation in genes encoding the epithelial cell-derived cytokines, interleukin-33 (IL-33) and thymic stromal lymphopoietin (TSLP), and the IL1RL1 gene encoding the IL-33 receptor, ST2, highlight the central roles for innate immune response pathways that promote the activation and differentiation of T-helper 2 cells in the pathogenesis of both asthma and allergic diseases. In contrast, variation at the 17q21 asthma locus, encoding the ORMDL3 and GSDML genes, is specifically associated with risk for childhood onset asthma. These and other genetic findings are providing a list of well-validated asthma and allergy susceptibility genes that are expanding our understanding of the common and unique biological pathways that are dysregulated in these related conditions. Ongoing studies will continue to broaden our understanding of asthma and allergy and unravel the mechanisms for the development of these complex traits. Author Affiliation: (1)Department of Human Genetics, The University of Chicago, Chicago, IL, USA. (2)Division of Allergy, Asthma, and Rheumatology, Department of Pediatrics, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taoyuan, Taiwan. Article note: Carole Ober, Department of Human Genetics, The University of Chicago, 920 E. 58th Street, CLSC 425, Chicago, IL 60637, USA, Tel.: +1 773 834 0735, Fax: +1 773 834 0505, e-mail: firstname.lastname@example.org
Childhood Asthma -- Genetic Aspects ; Allergy -- Genetic Aspects ; Disease Susceptibility -- Genetic Aspects ; Genomics
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