Gene–gene interaction between IL-13 and IL-13Rα1 is associated with total IgE in Korean children with atopic asthma View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2006-11-20

AUTHORS

Hyo-Bin Kim, Yong-Chul Lee, So-Yeon Lee, Jongsun Jung, Hyun-Seung Jin, Ja-Hyeung Kim, Bong-Seong Kim, Mi-Jin Kang, Seong-Ok Jang, Jihong Kim, Kuchan Kimm, Eun-Soon Shin, Seong-Gene Lee, Soo-Jong Hong

ABSTRACT

Interleukin (IL)-13, which is essential for IgE synthesis, mediates its effects by binding with a receptor composed of IL-4Ralpha and IL-13Ralpha1. We investigated the effects of IL-13 and IL-13Ralpha1 polymorphisms in Korean children with asthma, and whether these have been associated with IgE production. We enrolled 358 atopic asthmatic, 111 non-atopic asthmatic, and 146 non-atopic healthy children. IL-13 and IL-13Ralpha1 genotypes were identified using the PCR-RFLP method. There was an association between the asthma susceptibility and homozygosity for risk allele of IL-13 G+2044A. In children with atopic asthma, risk alleles in IL-13 (A-1512C and C-1112T) and IL-13Ralpha1 (A+1398G) showed increased total IgE (P=0.012, 0.015 and 0.017, respectively). Three-loci haplotype analysis for IL-13 showed that the haplotype composed of -1512C, -1112T and +2044A was associated with higher total IgE than other tested haplotypes in children with atopic asthma (P=0.003). The gene-gene interaction between risk alleles of each IL-13 promoter polymorphism and IL-13Ralpha1 polymorphism was associated with higher total IgE in children with atopic asthma (P=0.002, 0.010). These findings indicate that the IL-13 G+2044A is associated with asthma development and the IL-13 and IL-13Ralpha1 polymorphisms may interact to enhance IgE production. More... »

PAGES

1055

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10038-006-0061-x

DOI

http://dx.doi.org/10.1007/s10038-006-0061-x

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1001906476

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17006604


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