Expression of Toll-like receptors 7 and 9 as well as their regulatory molecules myeloid differentia-tion factor 88 and nuclear factor-κB in peripheral blood mononuclear cells of patients with vitiligo

Yaping Tang; Wenting Sheng; Xin Zhou; Xiaodong LI; Xin Tian; Jinbao Zhong; Zhenjie LI; Chunsheng Lin; Yumei Liu

Return

Expression of Toll-like receptors 7 and 9 as well as their regulatory molecules myeloid differentia-tion factor 88 and nuclear factor-κB in peripheral blood mononuclear cells of patients with vitiligo

VernacularTitle:Toll样受体7、9及其调控分子MyD88、NF-κB在白癜风患者外周血单个核细胞中的表达
Author: Yaping TANG ; Wenting SHENG ; Xin ZHOU ; Xiaodong LI ; Xin TIAN ; Jinbao ZHONG ; Zhenjie LI ; Chunsheng LIN ; Yumei LIU
Keywords: Vitiligo; Toll-like receptor 7; Toll-like receptor 9; Myeloid differentiation factor 88; NF-kappa B
From: Chinese Journal of Dermatology 2017;50(1):13-17
CountryChina
Language:Chinese
Abstract: Objective To compare expression of Toll?like receptors 7 and 9(TLR7, TLR9)as well as their regulatory molecules myeloid differentiation factor 88(MyD88)and nuclear factor?κB(NF?κB)in peripheral blood mononuclear cells(PBMCs)between patients with vitiligo and healthy individuals, and to explore their significance. Methods Flow cytometry was performed to measure expression of TLR7 and TLR9 in PBMCs among 36 patients with vitiligo and 22 healthy controls, and real?time fluorescence?based quantitative PCR(RT?PCR)was conducted to determine mRNA expression of MyD88 and NF?κB in the above blood samples. Results Compared with healthy controls, patients with vitiligo showed higher expression of TLR7 and mRNA expression of MyD88 and NF?κB, but lower expression of TLR9. However, significant differences were only observed in the mRNA expression of NF?κB(t=2.814, P=0.008), but not in the expression of TLR7 and TLR9 or the mRNA expression of MyD88 between patients and controls (t = 1.477, 1.761, 0.058, all P > 0.05). Conclusion NF?κB, as a key signaling molecule of TLR7 and TLR9 regulation pathways, increases obviously in patients with vitiligo, suggesting that NF?κB may be involved in the pathogenesis of vitiligo.