Zhang Na, Zhang Jing, Tan Ya-Qin, Du Ge-Fei, Lu Rui, Zhou Gang
The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, People's Republic of China.
The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, People's Republic of China; Department of Oral Medicine, School and Hospital of Stomatology, Wuhan University, Wuhan, People's Republic of China.
Int Immunopharmacol. 2017 Jul;48:84-90. doi: 10.1016/j.intimp.2017.04.016. Epub 2017 May 5.
Oral lichen planus (OLP) is a chronic inflammatory disease regulated by T cell-mediated immune response. Autophagy and its major inhibitory pathway Akt/mTOR participate in T cell metabolism and homeostasis, which has been implicated in autoimmune diseases. In this study, the potential involvement of autophagy and its regulatory Akt/mTOR pathway were investigated in local T cells of OLP. The expression of Akt/mTOR pathway and autophagy-related proteins in OLP local lesions, as well as in T cells, were measured by immunohistochemistry and double-labeling immunofluorescence, respectively. Furthermore, the associations of p-Akt, p-mTOR, ULK1, and LC3B expression with RAE scores representing the disease severity of OLP were assessed. The expression of p-Akt, p-mTOR, ULK1, and LC3B in OLP lesions, as well as in local T cells, was significantly increased compared with that in controls. In addition, the level of LC3B was negatively correlated with RAE scores of OLP, and LC3B was higher in nonerosive OLP than erosive ones and controls. Our results suggested that activated Akt/mTOR-autophagy may have a role in the local T cell-mediated immunoregulatory mechanism of OLP. LC3B might be a valuable marker to monitor the disease severity of OLP.
口腔扁平苔藓（OLP）是一种由T细胞介导的免疫反应调节的慢性炎症性疾病。自噬及其主要抑制途径Akt/mTOR参与T细胞代谢和内环境稳态，这与自身免疫性疾病有关。在本研究中，研究了自噬及其调节性Akt/mTOR途径在OLP局部T细胞中的潜在作用。分别通过免疫组织化学和双标免疫荧光法检测OLP局部病变以及T细胞中Akt/mTOR途径和自噬相关蛋白的表达。此外，评估了p-Akt、p-mTOR、ULK1和LC3B表达与代表OLP疾病严重程度的RAE评分之间的相关性。与对照组相比，OLP病变以及局部T细胞中p-Akt、p-mTOR、ULK1和LC3B的表达显著增加。此外，LC3B水平与OLP的RAE评分呈负相关，且非糜烂性OLP中的LC3B高于糜烂性OLP和对照组。我们的结果表明，激活的Akt/mTOR-自噬可能在OLP局部T细胞介导的免疫调节机制中起作用。LC3B可能是监测OLP疾病严重程度的一个有价值的标志物。
