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目的:分析多发性硬化(MS)进展型患者不同表型NK细胞亚群对临床主要治疗方法的反应性差异。方法:分离患者外周血中的NK细胞,以流式细胞术根据表面抑制性受体CD94/NKG2A表达情况分为两个亚群CD94/NKG2A-bright和CD94/NKG2A-dim。分别加入IFN-β,测定两个亚群表面CD94/NKG2A变化及细胞增殖,同时检测两种亚群分泌IL-10和TGF-β情况。结果:CD94/NKG2A阳性表达的NK细胞占25.5%,其中CD94/NKG2A-bright和CD94/NKG2A-dim分别占其中的23.6%和76.4%。加入IFN-β,CD94/NKG2A-bright组增殖率明显低于CD94/NKG2A-dim组,CD94/NKG2A表达峰度变化不大。CD94/NKG2A-dim组中CD94/NKG2A表达显著增加。两个亚群分泌的IL-10和TGF-β与未刺激组相比,均有明显差异。CD94/NKG2A-bright和CD94/NKG2A-dim组间亦有明显差异。结论:IFN-β通过诱导NK细胞CD94/NKG2A表达在非特异免疫系统中抑制NK细胞;同时刺激IL-10和TGF-β分泌进一步发挥对免疫系统的抑制。CD94/NKG2A-bright和CD94/NKG2A-dim对IFN-β反应有差异性。
OBJECTIVE: To analyze the difference of reactivity of different phenotype NK cell subsets in patients with multiple sclerosis (MS) with advanced clinical treatment. Methods: The NK cells in peripheral blood of patients were separated and divided into two subsets of CD94 / NKG2A-bright and CD94 / NKG2A-dim according to the expression of surface inhibitory receptor CD94 / NKG2A by flow cytometry. IFN-β was added separately, and the changes of CD94 / NKG2A and cell proliferation on the two subpopulations were determined. Meanwhile, the levels of IL-10 and TGF-β secreted by the two subpopulations were detected. Results: CD94 / NKG2A positive NK cells accounted for 25.5%, of which CD94 / NKG2A-bright and CD94 / NKG2A-dim accounted for 23.6% and 76.4% of them, respectively. The proliferation rate of IFN-β and CD94 / NKG2A-bright group was significantly lower than that of CD94 / NKG2A-dim group, and the expression of CD94 / NKG2A did not change much. CD94 / NKG2A expression was significantly increased in the CD94 / NKG2A-dim group. IL-10 and TGF-β secreted by both subgroups were significantly different from those in unstimulated group. There was also a significant difference between the CD94 / NKG2A-bright and CD94 / NKG2A-dim groups. CONCLUSION: IFN-β can inhibit NK cells in non-specific immune system by inducing CD94 / NKG2A expression in NK cells. At the same time, IFN-β can stimulate the secretion of IL-10 and TGF-β to further suppress the immune system. Differences in IFN-β response between CD94 / NKG2A-bright and CD94 / NKG2A-dim.