适应性免疫紊乱是重症COVID-19炎症风暴发生的关键因素。我们既往研究已从细胞水平上确定CD200影响机体适应性免疫应答特别是Th1、Th17、Treg细胞效应发挥负向免疫调节作用； 我们还发现CD200Fc与NaïveT细胞共孵育上清液富含TGF-β，后者是Treg主要效应因子，可以促进Treg细胞分化表达，影响Th17细胞定向分化。此外，芍药苷可以上调CD200以及TGF-β表达，提示：芍药苷可能桥接CD200与TGF-β间的免疫关联继而调控机体适应性免疫应答，只是芍药苷在其中的具体机制仍不清楚。本课题据此“执果索因”，从细胞、分子水平研究芍药苷调控CD200与TGF-β信号间的crosstalk对COVID-19适应性免疫应答影响，阐明新冠病毒感染后机体抗炎与促炎免疫紊乱的机制及下游信号转导，探索芍药苷作为靶向COVID-19炎症风暴抗炎药物的理论依据，为临床决策提供新依据。

It was revealed that immunodeficiency including abberant expression of Th17 and Treg cells worsen the progression of inflammatory storm in COVID-19, and significantly correlated with severity of clinical symptoms, illustrating that abnormal polarization and function of Th17 and Treg cells play pivotal role in the irritability immunopathogenesis of serious COVID-19. . Our preliminary study has demonstrated that CD200Fc significantly inhibit proliferation of human CD4+T cells, decrease differentiation of Th1 cells and Th17 cells cells, whereas increase differentiation of Treg cells. Moreover，The induced Treg cells may contribute to influence from the polarization to the phenotype of CD4+T cell subtypes. All these evidences collectively indicate that CD200 itself as a pivotal anti-inflammatory intervention particularly in immune response of Th17 cells including the production of its cytokines. In addition, our study has also found that Paeoniflorin could promote CD200 expression on human CD4+T cells and TGF-β expresstion as well . . Given CD200 and TGF-β has an immunoregulatory effects of immune CD4+T cells, maintaining immune homeostasis, highlighting themselves as potential anti-inflammatory intervention in immune-related diseases. However, information on the relationship among Paeoniflorin and CD200 and TGF-β pathway in abberant immunopathogenesis induced by novel coronavirus-19 is very limited. . In this study, we will systematically investigate the role of Paeoniflorin on regulation between CD200/CD200R1 and TGF-β Signaling pathways in immunopathologic aberrance induced by novel coronavirus-19, particularly in the effect toward Th17 and Treg phenotype polarization and function, so as to explore if Paeoniflorin is a potential anti-inflammatory treatment target in novel coronavirus-19 induced immunopathologic aberrance.