Abstract
Purpose: :
Interleukin–13 (IL–13), like IL–4, that is producing by Th2 type helper T cells, mast cells and basophils has been thought to be important in the development of allergic disease and atopy. IL–13 signaling is mediated by the type–2 IL–4 receptor, which consists of the IL–4 receptor (IL–4R) and IL–13 receptor alpha 1 chains (IL–13Ra1). However, another IL–13–binding chain, IL–13R alpha 2 (IL–13Ra2), appears to strongly inhibit the activity of IL–13. This study was attempted to investigate whether is diffethe expression of IL–13Ra2 on normal or AKC patient derived conjunctival fibroblasts was altered.
Methods: :
Conjunctival fibroblasts derived non–allergic donor (NF, n=3) and allergic conjunctivitis patients (AF, n=3) were cultured in the same conditions. These fibroblasts were stimulated with or without IL–4 and TNF–alpha (30 ng/ml), and the expression of IL–4R, IL–13Ra1 and IL–13Ra2 were examined by Quantitative Real–time PCR and flow cytometric analysis, respectively.
Results: :
Real–time quantitative PCR and flow cytometric analysis revealed that both mRNA and protein of IL–13Ra2 were upregulated by IL–4/IL–13 and TNF–alpha in NF, whereas the expression level of the IL–13Ra2 was relatively low in AF. The expression of IL–4R and IL–13Ra1, which were involved in IL–4 and IL–13 signaling, were not altered significantly between NF and AF.
Conclusions: :
The impaired IL–13Ra2 in AF may possibly be caused the amplification of IL–13 signaling and contribute to the pathogenesis of allergic keratoconjunctivitis.
Keywords: cytokines/chemokines • conjunctiva