Treatment strategy of oral mucosal disease that targeted thecontrol factor SOCS of JAK / STAT

本研究从免疫学-分子生物学水平对SOCS参与炎症细胞因子激活STAT和TLR介导的天然免疫衰竭进行了功能分析，以治疗被认为是天然免疫衰竭引起的口腔黏膜疾病。特别是阐明细胞因子和Th 17、Treg在口腔黏膜疾病（白斑、扁平苔藓）中的控制机制及其发病机制。我去寻找相关因子在Th 17，Treg口腔癌，扁平苔藓，在每一个口腔粘膜疾病从白斑。IL-6、TNFα、IL-23在白斑中表达上调。用RT-PCR方法检测Th 17、Treg、RORγt、Foxp 3、GATA 3、T-bet的表达，进一步分别观察到明显差异。我没有抓住Th 17的明显特征和定位。有必要进一步考虑。

In this study, we carried out in immunologically-molecularbiological level functional analysis involvement of SOCS to activation of STAT byinflammatory cytokines and collapse of innate immunity via TLR for performing thetreatment of disease of the oral mucosa which is assumed to be caused by failure ofinnate immunity. In particular, it aimed to elucidate control mechanism (leukoplakia,lichen planus) of the oral mucosa diseases caused by cytokines and Th17, Treg, themechanism of pathogenesis in this application. I went to search for associated factorsin Th17, Treg oral cancer, lichen planus, in each oral mucosal disease fromleukoplakia. Upregulation IL6, TNFα, the IL-23 was observed in leukoplakia. ForTh17, Treg, expression RORγt, the Foxp3, was investigated by RT-PCR method ofexpression, GATA3 T-bet further respectively obvious difference was observed. I didnot grasp the obvious feature also localization of Th17. And it will be necessary toconsider further forward.