紫杉醇通过上调TAP-1, TAP-2以及消除调节性T细胞逆转肺癌免疫逃逸

BACKGROUND AND OBJECTIVE: Until now, there are still some questions that chemotherapy could block cancer immunologic escape or not. The aim of this study is to explore the mechanism of paclitaxel in the blocking of immunologic escape in 3LL bearing mice. METHODS: MHC class I components were detected by FACS antibodies TAP-1 and TAP-2 in 3LL group and 3LL pretreated with 5×10(-8) mmol/L paclitaxel. C57BL/6 mice were divided into 3 groups: tumor –bearing group, paclitaxel-treating group and tumor-free group. 3LL cells (0.3×10(6)) were injected via tail vein of mice. On day 8, paclitaxel (0.012 5 mg) was injected subcutaneously in the treatment group. On day 21, murine lung cells were suspended. With FACS triple staining, we analyzed expression of Treg in each group. RESULTS: The expression of TAP-1 (5.68%±0.65%), TAP-2 (89.54% ±4.8%) was remarkably higher in paclitaxel-pretreating 3LL group than that in 3LL bearing mice group with TAP-1 (1.93%± 0.25%), TAP-2 (67.78%±5.08%), P=0.006, P=0.036 respectively. The expression of regulatory T cells (Treg) in tumor bearing mice was significantly higher (25.46%±2.23%) than that of in normal mice (12.46%±1.21%) (P < 0.001). Expression of Treg in paclitaxel treated mice was remarkably inhibited (17.53%±1.24%) compared with that in 3LL bearing mice group (P=0.004). CONCLUSION: Paclitaxel may block immunologic escape in the treatment of 3LL bearing mice partly through up-regulation TAP-1, TAP-2 and eliminatiing Treg cells.