目的 探讨辅助性T细胞17（T helper cell 17，Th17）对急性B淋巴细胞白血病（B cell-acute lymphoblastic leukemia， B-ALL）进展的影响及可能的作用机制。 方法 构建B-ALL小鼠模型。采用流式细胞术检测B-ALL小鼠外周血、骨髓、脾脏和淋巴结Th17细胞的比例。进一步通过细胞因子芯片分析B-ALL小鼠外周血细胞因子的表达情况，采用ELISA验证B-ALL小鼠外周血细胞IL-17A的表达。Th17细胞与白血病细胞共培养，通过流式细胞术检测Ki-67阳性细胞和B-ALL细胞凋亡比例，分析B-All细胞对Th17细胞的招募作用；通过Westernblot检测凋亡相关蛋白的表达。通过体内人急性白血病小鼠模型评价Th17细胞通过分泌IL-17A 促B-ALL进展。 结果 Th17细胞在B-ALL小鼠外周血（P < 0.000 1）、骨髓（P < 0.000 1）、脾脏（P < 0.000 1）和淋巴结（P < 0.000 1）中升高。IL-17A在B-ALL模型小鼠外周血中表达升高（P < 0.000 1），Th17细胞通过IL-17A促进B-All细胞增殖（P < 0.000 1），抑制其凋亡（P < 0.000 1）。B-All细胞通过CXCL16招募Th17细胞（P < 0.000 1）。体内动物实验结果表明，IL-17A处理显著增加了人急性白血病小鼠外周血、骨髓和脾脏中的白血病细胞比例，并缩短其生存时间。 结论 Th17细胞在B-ALL中比例升高，B-All细胞通过CXCL16招募Th17细胞，Th17细胞分泌IL-17A 促B-All进展。

Objective To investigate the effect of T helper cell 17（Th17）on the progression of B cell?acute lymphoblastic leukemia （B?ALL）and its possible mechanism. Methods We established the B?ALL mouse model and detected the proportion of Th17 cells in peripheral blood， bone marrow， spleen and lymph nodes by flow cytometry. Further， we used cytokine microarray to analyze the expression of cytokine in peripheral blood of B?ALL mice， and used ELISA to verify the IL?17A expression in peripheral blood of B?ALL mice. Th17 cells were co?cultured with leukemia cells， and the apoptosis ratio of Ki?67 positive cells and B?ALL cells was detected by flow cytometry， the recruitment effect of B?All cells on Th17 cells was analyzed. The expression of apoptosis?related proteins was detected by Western blot. The development of B?ALL by secreting IL-17A from Th17 cells was evaluated in vivo in a mouse model of human acute leukemia. Results Th17 cells were increased in peripheral blood（P < 0.000 1）， bone marrow（P < 0.000 1）， spleen （P < 0.000 1） and lymph nodes （P < 0.000 1） of B?ALL mice. The expression of IL?17A was increased in peripheral blood of B?ALL model mice （P < 0.000 1）， and Th17 cells promoted the proliferation of B?All cells and inhibited their apoptosis through IL?17A （P < 0.000 1）. B?All cells recruit Th17 cells through CXCL16（P < 0.000 1）. The animal experiments showed that IL?17A treatment significantly increased the proportion of leukemia cells in peripheral blood， bone marrow and spleen of B?ALL mice， and shortened their survival time. Conclusion The proportion of Th17 cells in B?ALL increases， B?All cells recruit Th17 cells through CXCL16， and Th17 cells secrete IL-17A to promote B?All progression.