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A. Matsuda, H. HItora, J. Hamuro, S. Kinoshita; Functional Analysis of IL-33 in Human Corneal Epithelial Cells. Invest. Ophthalmol. Vis. Sci. 2008;49(13):436. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
Interleukin-33 (IL-33) is a novel cytokine, inducing prominent Th2 dominant, eoshinophilic inflammation in the lungs and skin. Recently, the IL-33 hetero-dimmer receptor was identified as ST2L, one of the atopy related molecules, and as IL-1 receptor beta. We previously reported IL-33 mRNA expression in human corneal and conjunctival epithelium (ARVO, 2006). We investigated the regulation of IL-33 expression and its down-stream signaling pathway in human ocular surface epithelium.
The expression of IL-33 mRNA in human corneal epithelial cells (HCE) was quantified with real-time PCR with various inflammatory stimuli. The effect of recombinant IL-33 (rIL-33) on HCE was examined by phospho-p38 MAPK expression. The intensity of the NF-kB signal was quantified with luciferase assay using HCE, with IL-33 receptor (ST2L) over-expression or its decoy receptor (soluble ST2: sST2) over-expression.
Constitutive IL-33 mRNA expression was observed in HCE cells and its expression was up-regulated with interferon gamma stimulation. rIL-33 stimulation induced phospholylation of p38 MAPK, and increased NF-kB signals in HCE. ST2L over-expression enhanced NF-kB signals in HCE, whereas sST2 over-expression blocked NF-kB activation signals through IL-33 stimulation.
IL-33 stimulation activates HCE through the p38 MAPK and NF-kB pathways. The soluble ST2 molecule is a counter regulatory molecule for this pathway like the IL-1 receptor agonist for IL-1 pathways.
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