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.
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.