CD137信号通路对CD3−CD56+NK细胞功能影响的研究

Yu Zhang, Songwen Ju, Yongqian Shu
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引用次数: 2

摘要

目的探讨CD137信号通路对CD3 - CD56+NK细胞功能的调控作用。方法用CD137单抗或小鼠IgG1同型对照处理scd3 - CD56+NK细胞,研究CD137信号通路对CD3 - CD56+NK细胞功能的影响。采用细胞培养上清LDH活性测定细胞毒性;流式细胞术检测NKG2D和LFA-1在CD3−CD56+NK细胞中的表达。结果scd137在活化的CD3−CD56+NK细胞上表达。CD137单抗增强了CD3−CD56+NK细胞杀死肺癌细胞的能力(A549);进一步研究发现,活化细胞中NKG2D和LFA-1的表达显著增加,阻断NKG2D和LFA-1可显著减弱A549癌细胞的CD3 - CD56+NK细胞溶解。结论cd137信号通路通过上调NKG2D和LFA-1的表达,增强了CD3 - CD56+NK细胞杀伤癌细胞的能力。
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Research on the effects of CD137 signaling on the function of CD3−CD56+NK cells

Objective

To investigate the effects of CD137 signaling on the regulation of CD3CD56+NK cells function.

Methods

CD3 CD56+NK cells were treated with CD137 mAb or mouse IgG1 isotype control to study the effects of CD137 signaling on the function of CD3CD56+NK cells. Cytotoxicity was measured by LDH activity in the supernatants of cell cultures; NKG2D and LFA-1 expression on CD3CD56+NK cells were analyzed by flow cytometry.

Results

CD137 was expressed on activated CD3CD56+NK cells. The CD137 mAb enhanced the ability of CD3CD56+NK cells to kill lung cancer cells(A549); Further studies revealed that the expression of NKG2D and LFA-1 was significantly increased in activated cells, and blockade of NKG2D and LFA-1 dramatically attenuated CD3CD56+NK cytolysis of A549 cancer cells.

Conclusion

CD137 signaling increases the ability of CD3CD56+NK cells to kill cancer cells via up-regulating the expression of NKG2D and LFA-1.

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