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作 者:刘玉梅[1] 王化泉[1] 邵宗鸿[1] LIU Yu-Mei;WANG Hua-Quan;SHAO Zong-Hong(Department of Hematology,Tianjin Medical University General Hospital,Tianjin 300052,China)
出 处:《中国实验血液学杂志》2025年第1期262-268,共7页Journal of Experimental Hematology
基 金:天津市教委科研计划项目(2022KJ235)。
摘 要:目的:探讨铁过载对小鼠T淋巴细胞表面程序性死亡受体-1(PD-1)表达的影响,以分析铁过载抑制T细胞功能的机制。方法:流式细胞术检测铁过载小鼠模型外周血T细胞内不稳定的铁池、活性氧以及T细胞表面PD-1的表达。结果:铁过载组小鼠T细胞内钙黄绿素平均荧光强度为2492±311.1,较对照组的3136±537.3明显降低(P<0.01),提示铁过载组小鼠T细胞内不稳定的铁池含量明显增高。与对照组相比,铁过载组小鼠外周血T细胞CD4/CD8比例正常或升高;铁过载组小鼠T细胞内活性氧水平为2452±393.3,较对照组的1874±121.8明显增加(P<0.001);铁过载组小鼠外周血T细胞表面PD-1表达明显升高,其中CD8+T细胞PD-1+比例为(12.97±6.92)%,对照组为(6.18±2.95)%(P<0.05);铁过载组小鼠外周血CD8-T细胞PD-1+比例为(33.55±15.69)%,对照组为(12.51±4.11)%(P<0.001)。结论:铁过载小鼠外周血T细胞表面PD-1表达明显升高,可能参与抑制T细胞效应功能。Objective:To investigate the effect of iron overload on the expression of programmed death-1(PD-1)on the surface of T lymphocyte in mice,in order to analyze the mechanism of iron overload inhibiting T cell function.Methods:Flow cytometry was used to detect the labile iron pool(LIP),reactive oxygen species(ROS),and the expression of PD-1 in peripheral blood T cells in mice with iron overload.Results:The mean fluorescence intensity of calcein in T cells of mice in iron overload group was 2492±311.1,which was significantly lower than 3136±537.3 in the control group(P<0.01),suggesting that increased LIP in iron overload group.Compared with the control group,the ratio of CD4/CD8 of peripheral blood T cells was normal or increased in iron overload group.The level of ROS in T cells was 2452±393.3 in iron overload group,which was significantly increased compared to 1874±121.8 in the control group(P<0.001).The expression of PD-1 on the surface of T cells was significantly increased.The percentage of PD-1+cells in CD8+T cells was(12.97±6.92)%and(6.18±2.95)%in iron overload group and control group,respectively(P<0.05),and that in CD8-T cells was(33.55±15.69)%and(12.51±4.11)%(P<0.001).Conclusion:The expression of PD-1 on peripheral blood T cells in mice with iron overload is significantly increased,which may be involved in inhibiting T cell effector function.
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