Fig. 1
Preparation of Vγ9Vδ2 T cells and their inhibition of glioblastoma in vitro and in vivo. A A total of 2 × 106 peripheral blood mononuclear cells (PBMCs) were obtained from healthy human donors and expanded using GMP-compliant serum-free medium containing bisphosphonate compounds and factors. Flow cytometry was performed to determine the purity of Vγ9Vδ2 T cells on day 10 after cultivation (n = 4). B Vγ9Vδ2 T cells were incubated with U-87MG-Luc, TJ905-Luc, or HTB15-Luc cells at different effective target (E:T) ratios of 0:1, 0.5:1, 1:1, or 3:1 in the presence of IL-2. The cell viability of GBM cells was determined by measuring luciferase activity after 18–20 h. Data are expressed as the mean ± standard deviation (SD). *P < 0.05, **P < 0.01, ***P < 0.001. C, D ELISA was performed to measure IFN-γ and TNF-α levels in the culture medium. Data are expressed as the mean ± SD. *P < 0.05, ***P < 0.001, ****P < 0.0001; n = 3. E An NSG mouse GBM model was established by intracerebroventricular injection of U87-MG-Luc cells. Mice were treated with Vγ9Vδ2 T cells or PBS (n = 8). A workflow diagram is shown. F MRI imaging was performed to visualize the tumor (red arrow). G Bioluminescence images of the mouse brain were taken on day 8, 12, and 19 after injection. H Bioluminescence intensity was measured to examine tumor growth. Data are expressed as the mean ± SD. ****P < 0.0001. I Kaplan-Meier survival analysis was performed