Vγ9Vδ2（γδ）T细胞具有独特的生物学特征，尤其在肿瘤免疫中。因为它具有MHC非限制性的细胞杀伤活性，且可以广泛的识别肿瘤细胞。然而，人们对于调控γδ T细胞杀伤活性的机制的了解还很匮乏。我们通过前期的研究发现，在人源化小鼠中，可以通过靶向性激活γδ T细胞从而控制Epstein-Barr病毒诱导的B淋巴细胞增殖性疾病。在此基础上，我们进一步发现激活后的γδ T细胞表达4-1BB分子，通过与其配体结合可以增强其杀伤能力，但其中的机制尚不清楚。我们由此提出假说，4-1BB/4-1BBL信号通路可能是调控Vγ9Vδ2 T细胞杀伤能力的重要机制。本研究拟利用人源化小鼠疾病模型深入探讨4-1BB在γδ T细胞介导的机体抗肿瘤免疫中的作用与机制，为更好地应用γδ T细胞于肿瘤生物治疗奠定坚实的理论基础。

The Vγ9Vδ2 (γδ) T cells have unique biological characteristics, particularly in tumor immunity. Because it has a non-MHC restricted cytotoxic activity, and can recognize a wide range of tumor cells. However, we are still far away from understanding the mechanism for the regulation of the cytotoxic activity of γδ T cells. Our previous findings showed that we could control the Epstein-Barr virus-induced B lymphocyte proliferative diseases (EBV-LPD) through boosting γδ T cells immunity. We further observed that the 4-1BB expressed on the activated γδ T cells can enhance the cytotoxic activity of γδ T cells through binding its ligand, but the mechanism is largely unknown. Thus, we hypothesized that 4-1BB/4-1BBL signaling pathway may play a very important role in the regulation of Vγ9Vδ2 T cell’s tumor-killing activity. In this study, we will further clarify the underlying mechanisms how the 4-1BB regulate the γδ T cell-mediated anti-tumor immunity in vivo by using the humanized mice with EBV-LPD and provide clue for tumor immune therapy.