胶质瘤是中枢神经系统最常见的原发性肿瘤，致残致死率高，预后极差。免疫共刺激分子B7H3在多种肿瘤组织中过度表达，并与肿瘤的生物学特性密切相关，被认为是一种新的肿瘤标志物和潜在的治疗靶点。既往B7H3功能研究主要集中于免疫调节功能，但越来越多的研究发现其免疫调节之外的新功能，我们前期研究证实B7H3表达和胶质瘤级别正相关，敲除B7H3可促进胶质瘤干细胞的分化，该过程可能受到TGF-β通路的调控。据此，我们推测B7H3不仅是胶质瘤免疫应答过程中的重要“媒介”，而且可作为肿瘤内源性分子生物学信号调节网络上的重要“节点”，参与胶质瘤的发生、发展过程。本课题拟首先探究B7H3在胶质瘤中表达及临床意义，然后解析B7H3在胶质瘤中的新功能和调控机制，最后结合体内外实验阐明B7H3介导化疗敏感性等的作用。预期结果可以揭示恶性胶质瘤中B7H3的作用机理，为胶质瘤新型免疫治疗提供靶点。

Glioma is the most common primary tumor in central nervous system with unfavorable outcome. Recent studies showed that B7 family proteins played an important role in malignant tumors, and B7 proteins could serve as an ideal target to treat tumors. As a new member of B7 family, the function of B7H3 is controversial. Our previous work demonstrated that B7H3 expression was positively correlated with glioma grade, and negatively correlated with prognosis. We also found that B7H3 favored its expression on tumor stem cells, and knockdown of B7H3 induced differentiation of tumor stem cells via the activation of TGF-β pathway. Accordingly, we proposed B7H3 as a mediator in glioma immune reaction and progression. Here, we will continue to investigate the clinical value of B7H3, the novel mechanism such as exosome, and the impact of B7H3 during chemotherapy. This project may discover novel target for future treatment modality and accelerate clinical translation of B7H3.