病毒性心肌炎（VMC）是青少年发生猝死和心衰的主要原因，目前其发病机制不清，因此临床上尚无有效的治疗措施。既往关于B细胞在VMC中的研究，主要集中在探讨B细胞分泌抗体，关于B细胞分泌细胞因子的研究甚少。而我们前期研究发现在小鼠VMC急性期，产生IL-10的B细胞显著升高，并且发现调节性B细胞可以抑制Th1细胞分泌IFN-γ。但关于B细胞及其分泌的细胞因子在VMC心肌损伤中的作用及机制尚未完全清楚。本项目用小鼠感染柯萨奇病毒B3建立VMC模型，揭示B细胞在VMC中的免疫学特征，探讨B细胞及其分泌的细胞因子在VMC中的变化。通过B细胞缺失小鼠，探讨B细胞缺失对小鼠VMC心肌损伤严重程度、疾病发展转归、抗体及相关细胞因子的影响，探讨B细胞及其分泌的细胞因子对Th1、Th2、Th17、Th22细胞发生和分化的影响及其机制。本项目的完成对进一步阐明VMC的机制和寻求VMC新的治疗靶点具有重要意义。

Viral myocarditis (VMC) is a primary cause of sudden death and heart failure in adolescent, but there is no effective treatment because its pathogenesis is not clear at present. Previous studies on B cells in VMC mainly concentrated on B cells producing antibody, but little was known on B cells producing cytokines. Our previous research showed that IL-10-producing B cells were increased in acute VMC, and showed that regulatory B cells could inhibit the Th1 cells from producing IFN-γ in VMC. However, the role and pathogenesis of B cells and B cell-derived cytokines in myocardial injury of viral myocarditis are not totally clear. In this study, we will investigate the immunological characteristics of B cells, and explore the changes of B cells and B cell-derived cytokines in VMC mice induced by Coxsackievirus B3. Using lack of B cells in mice, we aim to observe wether B cells will have an effect on myocardial injury, progression and prognosis of VMC, and the changes of antibodies and related cytokines in VMC. We will investigate the effects and mechanism of B cells and B cell-derived cytokines on generation and differentiation of Th1, Th2, Th17, Th22 cells in VMC. This work will be vital significance to further elucidate the mechanism of VMC and seek new treatment targets for VMC.