학술논문

Association between genes encoding components of the IL-4/IL-4 receptor pathway and dermatitis in children.
Document Type
Article
Source
Gene. Jul2014, Vol. 545 Issue 2, p276-281. 6p.
Subject
*INTERLEUKIN-4 receptors
*STAT proteins
*GENETIC polymorphisms
*SKIN inflammation
*JUVENILE diseases
*POLYMERASE chain reaction
*RESTRICTION fragment length polymorphisms
*GENETICS
Language
ISSN
0378-1119
Abstract
Abstract: Objective: To determine whether IL-4, IL-4Rα and STAT6 polymorphisms are associated with susceptibility to dermatitis in Egyptian children. Methods: We genotyped three groups of children, consisting of 106 atopic dermatitis (AD) children, 95 non-AD children, and 100 of healthy controls, for IL-4 (−590 C/T), (−33 C/T), IL-4Rα (I50V), (Q576R) and STAT6 (2964 G/A), (2892 C/T) gene polymorphisms using PCR-RFLP assay. Total serum IgE and serum IL-4 levels were detected by ELISA. Results: There was a non-significant association of IL-4 −590 C/T, −33 C/T polymorphisms in the children with non-AD or those with AD when compared with the controls. We identified a significant association between IL-4Rα I50V, Q576R polymorphisms and dermatitis susceptibility in AD (p=0.002, <0.001 respectively), whereas no such association was observed in non-AD group (p=0.52, 0.99 respectively). A significant association between STAT6 polymorphisms and both types of dermatitis was found. Patients who were carriers of IL4 −590C, IL-4Rα I50V G, STAT6 2964 A and STAT6 2892 T had an increased risk of AD [OR and 95% CI: 3.2 (2.5–4.2), p=0.005]. Furthermore, there was no relation between each polymorphism and serum IL-4 level (p>0.05 for each) while homozygosity for the risk alleles of IL-4, IL-4Rα and STAT6 SNPs were significantly associated with increased total IgE levels in all subjects. Conclusion: In Egyptian children, the IL-4Rα and the STAT6 polymorphism may play a role in susceptibility to AD. In addition, gene–gene interaction between the IL-4, the IL-4Rα and the STAT6 significantly increases an individual's susceptibility to AD. [Copyright &y& Elsevier]