IL-17 Regulated Expression of Psoriasis-related Factors from Human Keratinocytes
| Autor: | Yang Ya-Lan, 楊雅嵐 |
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| Rok vydání: | 2010 |
| Druh dokumentu: | 學位論文 ; thesis |
| Popis: | 98 Psoriasis is a chronic inflammatory skin disease clinically characterized by sharply demarcated erythematous plaques covered by silvery-white scales owing mainly to epidermal hyperproliferation and aberrant terminal differentiation of keratinocytes. In addition, arthropathy may associate with psoriasis in 5－20％ of the patients, making them have the burden of both mental and physical aspects. The pathogenesis of psoriasis is not yet clear, however, it may be associated with genetic and environmental factors. Recent studies indicate that the pathogenesis of psoriasis is connected with Type 17 helper T cell（Th17）. Th17 produce interleukin-17（IL-17）by the stimulation of interleukin-23（IL-23）, while IL-17 could induce IL-23 expression and further enhance the function of Th17. This vicious cycle may promote epidermal keratinocyte hyperprolifertion and result in clinical appearance of psoriatic lesions. Accordingly, this study was meant to focus on molecular mechanism of IL-17 regulate IL-23/p19 expression and wish to provide insight for therapy of psoriasis. Using reverse transcriptase polymerase chain reaction and western blot, we observed that IL-17A，IL-17F and TNF-α could individually up-regulate the expression of IL-23/p19 and other psoriasis-related factors on either mRNA and protein level. Moreover, the combination of IL-17A with either IL-17F or TNF-could regulate IL-23/p19 and psoriasis-related mRNA and protein level in different manner. Furthermore, curcumin could induce G2/M arrest and apoptosis detected by flow cytometry in HaCaT cells. Interestingly, IL-17A induced expression of p19 and psoriasis-related factors from HaCaT cells can be abolished by curcumin. Previous studies have demonstrated that IL-23/p19 expression can be induced by AP-1 activation, whereas curcumin is known to inhibit the transcriptional activity of AP-1. We suggest IL-17 may induce IL-23/p19 expression via activating AP-1-dependent pathway in keratinocytes. In the future, more experiments are await to further dissect and explore the molecule mechanism employed by IL-17 to regulate the expression of IL-23/p19 and other psoriasis-related factors. |
| Databáze: | Networked Digital Library of Theses & Dissertations |
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