Wu Kai-Xuan, Wang Xiao-Tong, Hu Xin-Lin, Jiang Xiao-Yong, Zhuang Jing-Cong, Xu Yan-Zhu, Lin Li-Rong, Tong Man-Li, Yang Tian-Ci, Liu Li-Li
Center of Clinical Laboratory, School of Medical, Zhongshan Hospital, Xiamen University, Xiamen, China.
Department of Dermatology, School of Medical, Zhongshan Hospital, Xiamen University, Xiamen, China.
Front Microbiol. 2021 Nov 30;12:749171. doi: 10.3389/fmicb.2021.749171. eCollection 2021.
Long non-coding RNAs are involved in many infectious diseases. Our previous studies showed that expression is increased in T lymphocytes of neurosyphilis patients compared to healthy controls. However, whether has biological functions remains unclear. The current study was undertaken to understand the mechanism of in T lymphocyte function in neurosyphilis patients. The pull-down assay showed that acted on the acetylase NAT10. The chromatin immunoprecipitation (ChIP)-PCR results showed that promoted the acetylation of histone H3K27 adjacent to the Kank1 promoter, thereby promoting Kank1 protein expression. Kank1 promotes 14-3-3 protein expression, inhibits NF-kB activation, inhibits IFN-γ secretion by T lymphocytes, and promotes T lymphocyte apoptosis. Taken together, our findings suggest a novel mechanism that upregulates to inhibit IFN-γ expression and promote T cell apoptosis in neurosyphilis.
长链非编码RNA参与多种感染性疾病。我们之前的研究表明,与健康对照相比,神经梅毒患者的T淋巴细胞中[具体长链非编码RNA名称]表达增加。然而,[具体长链非编码RNA名称]是否具有生物学功能仍不清楚。当前研究旨在了解[具体长链非编码RNA名称]在神经梅毒患者T淋巴细胞功能中的作用机制。下拉实验表明,[具体长链非编码RNA名称]作用于乙酰化酶NAT10。染色质免疫沉淀(ChIP)-PCR结果表明,[具体长链非编码RNA名称]促进Kank1启动子附近组蛋白H3K27的乙酰化,从而促进Kank1蛋白表达。Kank1促进14-3-3蛋白表达,抑制NF-κB激活,抑制T淋巴细胞分泌IFN-γ,并促进T淋巴细胞凋亡。综上所述,我们的研究结果提示了一种新机制,即[具体长链非编码RNA名称]上调[具体相关分子名称]以抑制神经梅毒中IFN-γ表达并促进T细胞凋亡。