背景：前期工作显示RA寒证患者表现为更严重的滑膜炎症，温经通络法治疗RA寒证有效，其机制与JAK/STAT通路有关，该通路受转录因子Egr2/Egr3调控，据此及文献进展提出假说：RA寒证生物学基础与Egr2/Egr3为核心的信号通路异常影响淋巴细胞增殖致免疫炎症有关。内容及方法:1 中医辨证指导下纳入RA寒证、热证患者及健康志愿者，行临床体征评价，外周血分离CD4+T细胞及血清，应用细胞学、分子生物学技术，通过分别与RA热证及健康志愿者比较，从Egr2/Egr3为核心的信号通路研究RA寒证的生物学特征及与临床相关性；2 Wistar大鼠建立CIA寒证模型，温经通络法干预，取外周血和滑膜，从Egr2/Egr3为核心的信号通路研究温经通络法的干预机制，与临床研究相呼应。通过以上研究，从Egr2/Egr3为核心的信号通路阐释RA寒证的生物学特征，丰富中医辨证的生物学机制，服务于临床诊治。

Basic research showed that inflammatory process of RA cold syndrome is more obvious,JAK/STAK signaling pathway is involed in the effects of WENJINGTONGLUO methods on RA cold syndrome.While Egr2/Egr3 can regulate the JAK/STAT signaling transfation.Basedon the above,the hypothesis is proposed:Egr2/Egr3 and its related imflammatory signaling pathway are involved in the biological basis of RA cold syndrome.The project is planned as following: ①Both RA patients with cold syndrome and heat syndrome,healthy volunteers will be selected,RA patients will be evaluated the clinical synptome,and all the selected person will be taken the blood samle.Cellular and molecular biology techniques will be used to explore the biological mechanisms of RA cold syndrome from Egr2/Egr3 and their related inflammatory signaling pathway; ② CIA cold syndrome model will be made with wistar rats.The rats will be treated with Wengjingtongluo medicine,then the blood and synovium samples will be taken, Cellular and molecular biology techniques will be used to explore the biological mechanisms of RA cold syndrome from Egr2/Egr3 and their related signaling pathway.With the research above,the RA cold syndrome biological mechanism will be analyzed from the point of transcription factor Egr2/Egr3,and used for the clinical diagnose and treatment.