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Background: Interleukin (IL) 13, a type 2 helper T cell (T(H)2), is an important regulator of inflammatory immune responses. It mediates its action through a receptor complex consisting of IL-13Ralpha1 and IL-4Ralpha. IL-13Ralpha2 binds IL-13 with high affinity and is thought to act primarily as a decoy receptor, sequestering IL-13 and thus inhibiting its action. Our aim was to clarify the role of these receptors in the diagnosis and follow-up of atopic patients., Methods: We genotyped the 1398A>G polymorphism in the IL-13Ralpha1 gene using restriction fragment length polymorphism for causal genetic diversity and measured serum levels of IL-13Ralpha2 in 105 atopic patients suffering from atopic asthma, atopic dermatitis, and atopic rhinitis (35 each). We compared the results with those of 35 nonatopic control individuals. Total immunoglobulin (Ig) E and serum IL-13Ralpha2 were measured using enzyme-linked immunosorbent assay, and the eosinophil counts were recorded., Results: A significant increase in serum IL-13Ralpha2 levels was recorded in the 3 atopic groups compared with the control group (P < .001), as well as a significant increase in total IgE levels and eosinophil counts. No significant association was found between 1398A>G and atopy other than a suggestive association between this polymorphism and raised total serum IgE levels in all 3 atopic groups (P < .001)., Conclusions: These findings indicate that IL-13Ralpha2 plays an important role in atopy and that increased levels in different groups highlight its regulatory role in the development of atopic symptoms. The 1398A>G polymorphism might be involved in the production of IgE.

Objectives: The aim of this study was to clarify the role of interferon (IFN) gamma in the diagnosis and follow-up of atopic patients. We genotyped the IFN-gamma polymorphism at position +874 to examine the relationship between serum levels of IFN-gamma and disease severity and the role of IFN-gamma as a biochemical and immunologic marker., Methods: The study population comprised 75 patients suffering from atopic asthma, atopic dermatitis, and allergic rhinitis (25 each), and 25 control participants. Total immunoglobulin (Ig) E and serum IFN-gamma were measured by enzyme-linked immunosorbent assay, the IFN-gamma polymorphism at position +874 was determined by amplification refractory mutation system-polymerase chain reaction, and eosinophil counts were recorded., Results: There was a significant association between genotype and the frequency of the A allele of the +874T/A polymorphism in atopic patients when compared with controls (P < .001). In all 3 groups, there was a significant increase in total IgE levels and eosinophil counts, and a decrease in serum IFN-gamma levels towards the presence of homozygous AA compared with homozygous TT., Conclusions: The IFN-gamma gene polymorphism at position +874 contributes to susceptibility to atopic diseases by decreasing the amount of IFN-gamma. Identification of variants of IFN-gamma gene signalling and its role in the development of atopic diseases provides a focus for the development of novel diagnostic and therapeutic strategies for these diseases.