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Abstract
The bioactivity of IL 13 a Th2 cytokine which is an important regulator of inflammatory immune responses is mediated through a receptor complex consisting of IL-13Rα1 and IL-4Rα chain which is very important in IL-13 and IL-4 dependent signaling. IL-13Rα2 binds IL-13 with high affinity which is thought to act primarily as a ‘‘decoy’’ receptor, sequestering IL-13 from the IL-13Rα1/IL-4Rα complex, and thus inhibiting its function. Our aim is to clarify the role of these receptors in the diagnosis and follow-up of atopic patients. Methods: We genotyped IL-13Rα1 polymorphism at position +1398A/G searching for a causal genetic diversity and measured serum level of IL-13Rα2 in 105 atopic patients suffering from atopic asthma, atopic dermatitis and atopic rhinitis (35 each) and compared the results to 35 non atopic control subjects. Total immunoglobulin (Ig) E and serum IL-13Rα2 were measured using enzyme-linked immunosorbent assay, The IL-13Rα1 polymorphism at position +1398A/G was determined by restriction fragment length polymorphism analysis (RFLP), and eosinophil count was recorded. Results: There was a significant increase in serum IL-13Rα2 in the three atopic groups when compared with controls (P<0.001). And there was a significant increase in total IgE levels and eosinophil counts. No significant association of +1398A/G polymorphism with risk of asthma or atopy was found apart from a suggestive association between the IL13Rα1 1398A>G and raised total serum immunoglobulin E levels in all atopic groups (P<0.001). Conclusions: These findings indicate that the interleukin-13 receptor α2 has a great role in the control of atopy and its increased level in different groups indicates its regulatory role in the development of atopic symptoms. The interleukin-13 receptor α1 subunit gene +1398A\G polymorphisms do not contribute to atopy susceptibility or severity, although the interleukin receptor α1 subunit gene locus might be involved in the control of immunoglobulin E production.