Human Umbilical Cord Mesenchymal Stem Cells Inhibit the Function of Allogeneic Activated Vγ9Vδ2 T Lymphocytes In Vitro.
Human Umbilical Cord Mesenchymal Stem Cells Inhibit the Function of Allogeneic Activated Vγ9Vδ2 T Lymphocytes In Vitro.
复制标题
人脐带间充质干细胞体外抑制同种异体激活Vγ9Vγ2 T淋巴细胞的功能
DOI：
10.1155/2015/317801
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发表时间：
2015
影响因子：
--
通讯作者：
Li H
中科院分区：
文献类型：
--
作者：
Liu X;Feng T;Gong T;Shen C;Zhu T;Wu Q;Li Q;Li H
背景资料。人脐带间充质干细胞(UC-MSCs)可以调节免疫细胞的功能。然而，UC-MSCs是否以及如何调节Vγ9Vδ2T细胞的功能尚不完全清楚。方法：研究方法。在有或无UC-MSCs存在的情况下，用帕米磷酸钠和白介素2(IL-2)激活和扩增PBMC或V-γ9Vδ-2T细胞。流式细胞仪检测UC-MSCs对V-γ-9V-δ-2T细胞增殖、细胞因子表达及细胞毒作用的影响。流式细胞仪检测UC-MSCs对Fas-L、表达TRAIL的V-γ9Vδ-2T细胞和V-γ9Vδ-2T细胞凋亡的影响。结果。UC-MSCs对V-γ-9V-δ-2T细胞增殖的抑制作用呈剂量依赖性和细胞接触非依赖性。与UC-MSCs共培养后，干扰素γ+细胞比例降低，颗粒酶B+Vγ9Vδ2T细胞比例增加。UC-MSCs抑制Vγ9Vδ2T细胞对H1N1流感病毒感染的A549细胞的杀伤作用，降低Vγ9Vδ2T细胞Fas-L+、TRAIL+T细胞的频率，但不能调节Vγ9Vδ2T细胞的凋亡。结论。提示UC-MSCs能有效抑制V-γ-9V-δ-2T细胞的增殖和细胞毒作用，并调节其细胞因子的产生。Fas-L和TRAIL参与了调控。细胞接触和V-γ-9V-δ-2T细胞的凋亡不是抑制的必要条件。
Background. Human umbilical cord mesenchymal stem cells (UC-MSCs) can regulate the function of immune cells. However, whether and how UC-MSCs can modulate the function of Vγ9Vδ2 T cells has not been fully understood. Methods. The PBMCs or Vγ9Vδ2 T cells were activated and expanded with pamidronate (PAM) and interleukin-2 (IL-2) with or without the presence UC-MSCs. The effects of UC-MSCs on the proliferation, cytokine expression, and cytotoxicity of Vγ9Vδ2 T cells were determined by flow cytometry. The effects of UC-MSCs on Fas-L, TRAIL-expressing Vγ9Vδ2 T cells, and Vγ9Vδ2 T cell apoptosis were determined by flow cytometry. Results. UC-MSCs inhibited Vγ9Vδ2 T cell proliferation in a dose-dependent but cell-contact independent manner. Coculture with UC-MSCs reduced the frequency of IFNγ+ but increased granzyme B+ Vγ9Vδ2 T cells. UC-MSCs inhibited the cytotoxicity of Vγ9Vδ2 T cells against influenza virus H1N1 infected A549 cells and also reduced the frequency of Fas-L+, TRAIL+ Vγ9Vδ2 T cells but failed to modulate the apoptosis of Vγ9Vδ2 T cells. Conclusions. These results indicated that UC-MSCs efficiently suppressed the proliferation and cytotoxicity of Vγ9Vδ2 T cells and modulated their cytokine production. Fas-L and TRAIL were involved in the regulation. Cell contact and apoptosis of Vγ9Vδ2 T cells were not necessary for the inhibition.