title: Discovering susceptibility genes for allergic rhinitis and allergy using a genome-wide association study strategy.
abstract: OBJECTIVE
  Allergic rhinitis and allergy are complex conditions, in which both genetic and environmental factors contribute to the pathogenesis. Genome-wide association studies (GWASs) employing common single-nucleotide polymorphisms have accelerated the search for novel and interesting genes, and also confirmed the role of some previously described genes which may be involved in the cause of allergic rhinitis and allergy. The aim of this review is to provide an overview of the genetic basis of allergic rhinitis and the associated allergic phenotypes, with particular focus on GWASs.
  
  
  RESULTS
  The last decade has been marked by the publication of more than 20 GWASs of allergic rhinitis and the associated allergic phenotypes. Allergic diseases and traits have been shown to share a large number of genetic susceptibility loci, of which IL33/IL1RL1, IL-13-RAD50 and C11orf30/LRRC32 appear to be important for more than two allergic phenotypes. GWASs have further reflected the genetic heterogeneity underlying allergic phenotypes.
  
  
  CONCLUSIONS
  Large-scale genome-wide association strategies are underway to discover new susceptibility variants for allergic rhinitis and allergic phenotypes. Characterization of the underlying genetics provides us with an insight into the potential targets for future studies and the corresponding interventions.
authors.affiliation: aDepartment of Otolaryngology Head and Neck Surgery, Beijing TongRen Hospital, Capital Medical University bBeijing Key Laboratory of Nasal Diseases, Beijing Institute of Otolaryngology cDepartment of Allergy, Beijing TongRen Hospital, Capital Medical University, Beijing, PR China *Jingyun Li and Yuan Zhang contributed equally to the writing of this article.
authors.forename: Jingyun
authors.initials: J
authors.lastname: Li
authors.forename: Yuan
authors.initials: Y
authors.lastname: Zhang
authors.forename: Luo
authors.initials: L
authors.lastname: Zhang
mesh_terms: D017766:Acid Anhydride Hydrolases; D000818:Animals; D045643:DNA Repair Enzymes / Q000235:genetics; D004268:DNA-Binding Proteins / Q000235:genetics; D020022:Genetic Predisposition to Disease; D055106:Genome-Wide Association Study; D006801:Humans; D007375:Interleukin-1 / Q000235:genetics; D018793:Interleukin-13 / Q000235:genetics; D000067596:Interleukin-33; D007378:Interleukins / Q000235:genetics; D008565:Membrane Proteins / Q000235:genetics; D011110:Polymorphism, Genetic; D053573:Receptors, Interleukin-1 Type I / Q000235:genetics; D065631:Rhinitis, Allergic / Q000235:genetics*
chemical_list: D004268:DNA-Binding Proteins; C508590:IL1R1 protein, human; C506536:IL33 protein, human; D007375:Interleukin-1; D018793:Interleukin-13; D000067596:Interleukin-33; D007378:Interleukins; C087215:LRRC32 protein, human; D008565:Membrane Proteins; D053573:Receptors, Interleukin-1 Type I; D017766:Acid Anhydride Hydrolases; C112158:RAD50 protein, human; D045643:DNA Repair Enzymes