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Background   IL13, IL4, IL4RA, FCER1B  and  ADRB2  are susceptible genes of asthma and atopy. Our previous study has found gene–gene interactions on asthma between these genes in Chinese Han children. Whether the interactions begin in fetal stage, and whether these genes interact with prenatal environment to enhance cord blood IgE (CBIgE) levels and then cause subsequent allergic diseases have yet to be determined. This study aimed to determine whether there are gene–gene and gene-environment interactions on CBIgE elevation among the aforementioned five genes and prenatal environmental factors in Chinese Han population.    Methods  989 cord blood samples from a Chinese birth cohort were genotyped for nine single-nucleotide polymorphisms (SNPs) in the five genes, and measured for CBIgE levels. Prenatal environmental factors were collected using a questionnaire. Gene–gene and gene-environment interactions were analyzed with generalized multifactor dimensionality methods.    Results  A four-way gene–gene interaction model ( IL13  rs20541,  IL13  rs1800925,  IL4  rs2243250 and  ADRB2  rs1042713) was regarded as the optimal one for CBIgE elevation (testing balanced accuracy = 0.5805,  P  = 9.03 × 10 –4 ). Among the four SNPs, only  IL13  rs20541 was identified to have an independent effect on elevated CBIgE (odds ratio (OR) = 1.36,  P  = 3.57 × 10 –3 ), while the other three had small but synergistic effects. Carriers of  IL13  rs20541 TT,  IL13  rs1800925 CT/TT,  IL4  rs2243250 TT and  ADRB2  rs1042713 AA were estimated to be at more than fourfold higher risk for CBIgE elevation (OR = 4.14,  P  = 2.69 × 10 –2 ). Gene-environment interaction on elevated CBIgE was found between  IL4  rs2243250 and maternal atopy (OR = 1.41,  P  = 2.65 × 10 –2 ).    Conclusions  Gene–gene interaction between  IL13  rs20541,  IL13  rs1800925,  IL4  rs2243250 and  ADRB2  rs1042713, and gene-environment interaction between  IL4  rs2243250 and maternal atopy begin in prenatal stage to augment IgE production in Chinese Han children.

Gene–gene and gene-environment interactions on cord blood total IgE in Chinese Han children