ERK1/2信号通路参与瘦素促人γδT细胞增殖调控

Role of ERK1/2 signal transduction system in the proliferation of γδT cells induced by leptin

为探讨ERK1/2信号通路在瘦素促进人γδT细胞增殖中的作用机制。我们用MTT法观察不同浓度瘦素促γδT细胞的增殖效应,以及用ERK1/2特异性抑制剂PD98059阻断ERK1/2信号通路对瘦素促细胞增殖效应的影响,Western blot法检测瘦素干预对ERK1/2、P-ERK1/2蛋白表达水平的影响。结果显示,瘦素在一定浓度范围内促进人γδT细胞增殖。瘦素可使ERK1/2信号通路中的靶蛋白发生磷酸化激活,用PD98059阻断ERK1/2信号通路可显著抑制瘦素促细胞的增殖效应,亦可抑制瘦素对γδT细胞ERK1/2蛋白磷酸化。因此,我们认为瘦素促人γδT细胞增殖效应可能与激活ERK1/2信号通路有关。

To explore the role ERK1/2 signal transduction system in the proliferation of human γδT cells induced by leptin,human γδT cells was treated with different concentrations of leptin,and the proliferation of γδT cells was measured by MTT assay.The expression of ERK,P-ERK was detected at different time of treatment with leptin by Western blotting with or without ERK1/2 signals blocked by PD98059,the inhibitor of ERK1/2.It was demonstrated that leptin could improve the proliferation of γδT cells in a concentration-dependent manner.As revealed by Western blotting,leptin induced the activation of ERK,and the expression of P-ERK1/2 in γδT cells was increased after leptin treatment.In addition,the proliferation activated by leptin after ERK1/2 signal pathway was blocked by their inhibitors,showing that after inhibition the activities of ERK and the proliferation induced by leptin was also attenuated.It is concluded that leptin can stimulate the proliferation of γδT cells in vitro and ERK1/2 signal transduction system may be involved in the proliferation of human γδT cells.