期刊
APOPTOSIS
卷 25, 期 9-10, 页码 663-673出版社
SPRINGER
DOI: 10.1007/s10495-020-01623-3
关键词
IL-22; Psoriasis; Anti-apoptosis; Keratinocytes; Bcl-xL; Bax
资金
- National Natural Science Foundation of China [81703130]
- Science and Technology Research and Development Program of Shaanxi Province of China [2016SF-238]
- Key Research and Development Program of Shaanxi Province of China [2019SF-147]
IL-22 is known to mediate inflammation in psoriasis, while IL-22 binding protein (IL-22BP) binds IL-22 to suppress IL-22 signaling. However, the function of IL-22 in regulating apoptosis in psoriasis remains poorly understood. In this study, we found that IL-22/IL-22R1 in lesional skin and IL-22 in serum from psoriatic patients were highly upregulated compared with healthy controls, while IL-22BP was not changed. Correlations between IL-22/IL-22R1 levels and the thickness of psoriatic lesions suggested that IL-22 might positively regulate abnormal hyperplasia in psoriasis. Apoptotic keratinocytes were increased only in stratum corneum, but not in spinous and basal layers of psoriasis. Moreover, IL-22 promoted cell viability in human epidermal keratinocytes (HEKs). The apoptosis induced by TNF-alpha and IFN-gamma was inhibited in HEKs treated with IL-22, since that IL-22 upregulated Bcl-xL and downregulated Bax production in HEKs in the presence of TNF-alpha and IFN-gamma. In addition, IL-22BP could counteract the anti-apoptotic effect of IL-22. Our finding demonstrates that IL-22 might play an anti-apoptosis role on keratinocytes to balance cell proliferation and apoptosis in psoriatic epidermis.
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