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本项目研究了21例CML患者,探讨热休克能否诱导CML细胞表达HSP70和促进自身T细胞对CML细胞的杀伤(ALK)活性,并了解γδT细胞与此活性的关系.结果显示热休克对CML靶细胞的自然释放率无影响.当E/T比为50:1时,T细胞对自身CML靶细胞具有不同程度的ALK活性,T细胞对自身未热休克的CML靶细胞的ALK活性为(9.32±12.78)%,而对自身热休克的CML靶细胞的ALK活性为(25.43±22.56)%(P<0.01).有12例患者对自身未热休克CML靶细胞的ALK活性为0,而对自身热休克CML靶细胞的ALK活性为(40.2±22.4)%.若以ALK活性>15.00%为阳性,则21例患者中仅有4例(19.05%)其T细胞对自身未热休克的CML靶细胞ALK阳性(33.13±9.67)%,但有10例(47.62%)患者T细胞对热休克后的CML靶细胞ALK阳性,活性为(43.80±17.39)%,两者有显著性差异(P<0.01).
This project studied 21 patients with CML to investigate whether heat shock could induce CML cells to express HSP70 and promote autologous T cell killing (ALK) activity on CML cells, and to understand the relationship between γδT cells and this activity. The results showed that heat shock to CML The natural release rate of target cells has no effect. When the E/T ratio is 50:1, T cells have ALK activity of different degrees to their own CML target cells, and the ALK activity of T cells to CML target cells that do not heat shock themselves is ( 9.32±12.78)%, while the ALK activity against self-heat shocked CML target cells was (25.43±22.56)% (P<0.01). There were 12 patients with ALK activity against their own unheat shocked CML target cells. The ALK activity of self-heat shocked CML target cells was (40.2±22.4)%. If the ALK activity was >15.00% positive, only 4 (19.05%) of the 21 patients had their T cells on their own heat shock. The positive rate of ALK in CML target cells was (33.13±9.67)%, but 10 (47.62%) patients had ALK positive for CML target cells after heat shock and the activity was (43.80±17.39)%. There was a significant difference between them ( P<0.01).