San-xiang Xie1, Lin Feng, Sheng-rong Zhu, Lei Ding. 1. Center of Stomatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology. Wuhan 430030;China.E-mail:xisix@163.com.
Abstract
PURPOSE: Oral lichen planus was considered as T cell mediated autoimmune disease affecting oral mucosa with unknown etiopathogenesis. Helper T lymphocytes played an important role in the pathogenesis of OLP. The purpose of this study was to investigate the possible role of Th17 and Treg cells in OLP lesions. METHODS: Forty three patients with OLP (24 patients with reticular OLP and 19 patients with atrophic-erosive OLP) and 13 healthy volunteers were recruited in this study. Real-time quantitative PCR was performed to detect the expressions of RORRORγT and FOXP3, which were the lineage-specific transcription factors for Th17 and Treg, respectively. Statistical difference was evaluated by GraphPad Prism 5 software. RESULTS: The results showed that the expressions of RORRORγT and FOXP3 in OLP lesions were significantly higher than that in normal oral mucosa, and correlated with the clinical classification of OLP. Additionally, it was found that RORRORγT/FOXP3 ratio in atrophic-erosive OLP was significantly higher than that in reticular OLP and control group; Moreover, increased RORRORγT/FOXP3 ratio in reticular OLP was found compared with control group, but the difference was not statistically significant. CONCLUSIONS: The results demonstrate that Th17 and Treg cells participate in the immune response in OLP lesions. Th17 predominance of Th17/Treg imbalance may implicate the immune response in atrophic-erosive OLP. These findings help to broaden our view on the pathogenesis of OLP.
PURPOSE: Oral lichen planus was considered as T cell mediated autoimmune disease affecting oral mucosa with unknown etiopathogenesis. Helper T lymphocytes played an important role in the pathogenesis of OLP. The purpose of this study was to investigate the possible role of Th17 and Treg cells in OLP lesions. METHODS: Forty three patients with OLP (24 patients with reticular OLP and 19 patients with atrophic-erosive OLP) and 13 healthy volunteers were recruited in this study. Real-time quantitative PCR was performed to detect the expressions of RORRORγT and FOXP3, which were the lineage-specific transcription factors for Th17 and Treg, respectively. Statistical difference was evaluated by GraphPad Prism 5 software. RESULTS: The results showed that the expressions of RORRORγT and FOXP3 in OLP lesions were significantly higher than that in normal oral mucosa, and correlated with the clinical classification of OLP. Additionally, it was found that RORRORγT/FOXP3 ratio in atrophic-erosive OLP was significantly higher than that in reticular OLP and control group; Moreover, increased RORRORγT/FOXP3 ratio in reticular OLP was found compared with control group, but the difference was not statistically significant. CONCLUSIONS: The results demonstrate that Th17 and Treg cells participate in the immune response in OLP lesions. Th17 predominance of Th17/Treg imbalance may implicate the immune response in atrophic-erosive OLP. These findings help to broaden our view on the pathogenesis of OLP.