暴发性肝炎发病机制复杂，缺乏行之有效的治疗手段。因此研究其发病机制具有十分重要的意义。前期我们已经利用鼠3型肝炎病毒（Mouse Hepatitis Virus-3, MHV-3）建立了暴发性肝炎小鼠模型，并且阐明了Clara细胞10-KDa蛋白（CC10）可以保护肝细胞的损伤，显著提高了暴发性肝炎小鼠的生存率，但其作用机制尚不明确。同时我们前期研究也证明了滤泡辅助性T细胞（Tfh）可加速肝细胞的损伤。我们推测CC10蛋白可能通过调控Tfh细胞进而预防肝损伤。本研究拟通过动物模型和细胞模型研究CC10蛋白对Tfh的调控作用及其机制，并通过体内过继转移CC10蛋白作用的Tfh或树突状细胞，进一步研究CC10对Tfh的调控及对疾病的保护作用。本研究试图阐明CC10对暴发性肝炎的保护作用及对Tfh的调控作用机制，从而为暴发性肝炎的防治奠定理论基础和提供潜在干预靶点。

The pathogenesis of fulminant hepatitis is complex and there is lack of effective treatment. We found that clara cell 10-KDa protein (CC10) could inhibit the progression of mouse fulminant hepatitis induced by Mouse Hepatitis Virus-3 (MHV-3), but its mechanism remains unclear. Our previous data also indicated that folicullar helper T cell (Tfh) cells were involved in the pathogenesis of fulminant hepatitis. We hypothesize that CC10 protein exerts its effect by regulating Tfh response. This study intends (1) to study the regulation of CC10 protein on Tfh cells in animal model and cells in vitro. (2) to further study the regulation of CC10 on Tfh in vivo by adoptive transfer of Tfh or dendritic cells treated with CC10 protein. This study aims to elucidate the regulation of CC10 on Tfh and possible mechanisms, and provide a new biological target and theoretical basis for the treatment of fulminant hepatitis.