title: Association of CARD15 polymorphisms with atopy-related traits in a population-based cohort of Caucasian adults.
abstract: BACKGROUND
  Influences of microbial pathogens are crucial for the maturation of the immune system. Caspase-recruitment domain containing protein 15 (CARD15) is a cytosolic receptor involved in bacterial recognition by antigen-presenting cells. CARD15 polymorphisms have been associated with Crohn's disease. Recently, associations with atopic phenotypes have been reported in children.
  
  
  OBJECTIVE
  Within a large population of German adults (n=1875), we evaluated eight CARD15 polymorphisms for associations with atopic phenotypes.
  
  
  METHODS
  Subjects were phenotyped by standardized questionnaires and interviews as well as total and allergen-specific IgE measurements. Genotyping was performed using matrix-assisted laser desorption ionization--time of flight mass spectrometry. Haplotypes were estimated using the SAS/Genetics module.
  
  
  RESULTS
  Subjects with a T allele at rs1077861 had a decreased risk of developing asthma (odds ratio OR=0.648, P=0.013), whereas the presence of an A allele at rs3135500 was significantly associated with an increased risk (OR=1.374, P=0.023). In addition, a CARD15 haplotype revealed to be protective against the development of asthma (OR=0.326, P=0.003). Subjects with an A allele at position rs5743266 or a T allele at rs2066842 had a significantly decreased risk of developing allergic rhinoconjunctivitis with ORs of 0.820 (P=0.049) and 0.801 (P=0.025). Polymorphism rs2066845 showed a significant association with increased total serum IgE (OR=2.155, P=0.006).
  
  
  CONCLUSIONS
  Genetic variants of CARD15 that might result in inappropriate immunomodulation are not only associated with autoimmune diseases but also with atopic disorders.
authors: Department of Dermatology and Allergy Biederstein, Technical University Munich, Germany.
authors: S
authors: S
authors: Weidinger
authors: N
authors: N
authors: Klopp
authors: L
authors: L
authors: Rümmler
authors: S
authors: S
authors: Wagenpfeil
authors: H J
authors: HJ
authors: Baurecht
authors: A
authors: A
authors: Gauger
authors: U
authors: U
authors: Darsow
authors: T
authors: T
authors: Jakob
authors: N
authors: N
authors: Novak
authors: T
authors: T
authors: Schäfer
authors: J
authors: J
authors: Heinrich
authors: H
authors: H
authors: Behrendt
authors: H E
authors: HE
authors: Wichmann
authors: J
authors: J
authors: Ring
authors: T
authors: T
authors: Illig
mesh_terms: D000483:Alleles; D001249:Asthma / Q000235:genetics; D015331:Cohort Studies; D003233:Conjunctivitis, Allergic / Q000235:genetics; D003430:Cross-Sectional Studies; D003876:Dermatitis, Atopic / Q000235:genetics; D005260:Female; D005838:Genotype; D006239:Haplotypes; D006801:Humans; D006967:Hypersensitivity / Q000235:genetics*; D007073:Immunoglobulin E / Q000097:blood; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics*; D015810:Linkage Disequilibrium / Q000235:genetics; D008297:Male; D008875:Middle Aged; D053473:Nod2 Signaling Adaptor Protein; D010641:Phenotype; D011110:Polymorphism, Genetic / Q000235:genetics*; D012220:Rhinitis / Q000235:genetics; D012307:Risk Factors
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; C429018:NOD2 protein, human; D053473:Nod2 Signaling Adaptor Protein; D007073:Immunoglobulin E