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作 者:汤海涛[1] 周玉斌[1] Tang Haitao;Zhou Yubin(The Second Department of Oncology,The People's Hospital of Liaoning Province,Shenyang 110001,China)
出 处:《国际免疫学杂志》2019年第6期575-578,共4页International Journal of Immunology
摘 要:目的:探讨白细胞介素(intedeukin,IL)-21及其受体IL-21R对小鼠急性肠炎调节机制.方法对照组使用9只C57BL/6小鼠,实验组使用9只IL-21R基因敲除小鼠,均禁食12 h,以4%三硝基苯磺酸(trinitro-benzene-sulfonic acid,TNBS)灌肠构建急性肠炎模型.流式细胞术法分析免疫细胞数量和比例.酶联免疫吸附法(enzyme-linked immuno sorbent assay,ELISA)测定细胞培养上清中IL-17、IFN-γ含量.结果与对照组小鼠相比,IL-21R基因敲除鼠体重下降缓慢(P<0.05),生存时间延长.与对照组相比,实验组肠道黏膜固有层淋巴细胞中CD4+T细胞比例[(43.72±3.06)%比(54.59±2.92)%],CD8+T细胞比例[(20.57±1.48)%比(30.39±2.21)%]和CD44+CD4+T细胞比例[(35.72±3.40)%(43.94±3.73)%]均下降(P值均<0.05),细胞培养上清中IL-17、干扰素(interfer-on,IFN)水平降低,差异均有统计学意义(P值均<0.05).结论IL-21/IL-21R通过调节T细胞亚群细胞比例和数量以及T细胞分泌的细胞因子水平促进TNBS诱导的肠炎进展.Objective To investigate the regulatory mechanism of interleukin(IL)-21 and its receptors on the progression of mouse colitis.Methods Nine C57 BL/6 male mice for control group,and nine IL-21R gene knockout male mice for experimental group.Mice were fasting for 12 h,treated with 4%trinitro-benzenesulfonic(TNBS)acid enema.The count and the proportion of immune cells were analyzed by flow cytometry.Levels of IL-17 and IFN in the supernatants were measured by enzyme-linked immuno sorbent assay(ELISA).Results Compared with the control group,the weight of the IL-21R knock-out mice decreased slowly(P<0.05),and the survival time was prolonged.Compare with the control group,the proportion of CD4+T cells,CD8+T cells and CD44+CD4+T cells in the colon mucosa of the experimental group all decreased[(43.72±3.06)%vs(54.59±2.92)%,(20.57±1.48)% vs(30.39±2.21)%and(35.72±3.40)%vs(43.94±3.73)%,all P<0.05],the levels of IL-17 and interferon(IFN) γ in the cell culture decreased(both P<0.05).Conclusion IL-21/IL-21R promotes the progression of colitis induced by TNBS by regulating the proportion and the number of T cell subsets and the amount of cytokines secreted by T cells.
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