title: Interaction of maternal atopy, CTLA-4 gene polymorphism and gender on antenatal immunoglobulin E production.
abstract: BACKGROUND
  Genetic heritability and maternal atopy have been correlated to antenatal IgE production, but very few studies have studied gene-maternal atopy interaction on antenatal IgE production. This study investigated the interaction of CTLA-4 polymorphism with prenatal factors on the elevation of cord blood IgE (CBIgE).
  
  
  METHODS
  Pregnant women were antenatally recruited for collection of prenatal environmental factors by a questionnaire. Umbilical cord blood samples were collected for CBIgE detection by fluorescence-linked enzyme assay and CTLA-4 polymorphism measurement by restriction fragment length polymorphism.
  
  
  RESULTS
  A total of 1104 pregnant women initially participated in this cohort study, and 898 of them completed cord blood collection. 21.4% of the newborns had elevation of CBIgE (>or=0.5 kU/L). The CTLA-4+49A allele (P=0.021), maternal atopy (P<0.001) and gender (P=0.034), but not the CTLA-4+49G allele, -318C allele, -318T allele, parental smoking or paternal atopy, were significantly correlated with the CBIgE elevation in multivariate analysis. A dichotomous analysis of gene-maternal atopy interactions identified maternal atopy and CTLA-4+49A allele had an additive effect on the CBIgE elevation, especially prominent in male newborns; and in the absence of maternal atopy, CTLA-4+49GG genotype had a protective effect on CBIgE elevation in female newborns.
  
  
  CONCLUSIONS
  Maternal but not paternal atopy has significant impacts on CBIgE elevation depending on gender and CTLA-4+49A/G polymorphism of newborns. Control of maternal atopy and modulation of CTLA-4 expression in the prenatal stage may be a target for the early prevention of perinatal allergy sensitization.
authors: Department of Pediatrics, Chang Gung Memorial Hospital - Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
authors: K D
authors: KD
authors: Yang
authors: C-Y
authors: CY
authors: Ou
authors: T-Y
authors: TY
authors: Hsu
authors: J-C
authors: JC
authors: Chang
authors: H
authors: H
authors: Chuang
authors: C-A
authors: CA
authors: Liu
authors: H-M
authors: HM
authors: Liang
authors: H-C
authors: HC
authors: Kuo
authors: R-F
authors: RF
authors: Chen
authors: E-Y
authors: EY
authors: Huang
mesh_terms: D015703:Antigens, CD / Q000235:genetics*; D000943:Antigens, Differentiation / Q000235:genetics*; D060908:CTLA-4 Antigen; D005220:Fathers; D005260:Female; D005312:Fetal Blood / Q000276:immunology; D020022:Genetic Predisposition to Disease; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000235:genetics* / Q000276:immunology; D007073:Immunoglobulin E / Q000096:biosynthesis*; D007231:Infant, Newborn; D008297:Male; D009035:Mothers; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length; D011247:Pregnancy; D011248:Pregnancy Complications / Q000235:genetics* / Q000276:immunology; D011297:Prenatal Exposure Delayed Effects; D012737:Sex Factors
chemical_list: D015703:Antigens, CD; D000943:Antigens, Differentiation; D060908:CTLA-4 Antigen; C556706:CTLA4 protein, human; D007073:Immunoglobulin E