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作 者:高庆贞[1] 王璞[1] 王琪[1] 姚小美[1] 王丽[1] 李进[1] 王小平[1] 徐何[2]
机构地区:[1]山东大学附属济南市中心医院肾脏病/血液净化中心,济南250013 [2]山东大学附属济南市中心医院移植科,济南250013
出 处:《山东大学学报(医学版)》2010年第6期45-48,共4页Journal of Shandong University:Health Sciences
基 金:济南市科技发展计划重大项目(200705089-8)
摘 要:目的研究单核细胞对异体血管内皮细胞(VEC)的活化作用以及产生干扰素诱导蛋白10(IP-10)、干扰素诱导的T细胞α型趋化因子(I-TAC)的效果。方法人外周血中分离单核细胞,酶消化法分离人主动脉内皮细胞,建立单核细胞与VEC共培养系统。用流式细胞仪(FACS)检测VEC表面粘附分子CD54、CD62E表达的情况,用RT-PCR检测VEC内I-TAC和IP-10mRNA的表达情况。结果 RT-PCR检测结果表明,VEC与同种异体单核细胞共培养24h后,细胞内IP-10和I-TACmRNA表达水平显著增加(P<0.05),且在48、72h的表达维持在较高的水平。FACS检测结果表明,正常培养的VEC少量表达CD54分子,不表达CD62E分子。与同种异体单核细胞共培养24h后,VEC表面CD62E和CD54的表达水平明显上调(P<0.05)。结论在同种异体单核细胞-血管内皮细胞免疫反应中,单核细胞能活化血管内皮细胞,使内皮细胞表达IP-10、I-TAC等趋化因子和CD54、CD62E等粘附分子,参与对移植器官的排斥反应。Objective To investigate the effects of endothelial cell activation as well as chemokines expression of IFN-γ-inducible protein 10 (IP-10) and IFN-γ-inducible T cell α chemo-attractant (I-TAC) initiated by allogeneic monocytes. Methods Human monocytes were isolated and purified from healthy human peripheral blood mononuclear cells and endothelial cells were isolated form human aortas. A co-cultured system of endothelial cells and allogeneic monocytes was established. Endothelial cells chemokine expression of IP-10 and I-TAC were analyzed by RT-PCR before and after co-culture. The level of CD54 and CD62E on endothelial cells was detected by florescence activated cell scanning (FACS). Results RT-PCR demonstrated that IP-10 and I-TAC mRNA levels markedly elevated at 24 hours( P0.05),remained at a high level at 48 hours and at 72 hours after co-culture(P0.05). FACS analysis revealed low level expression of CD54 and CD62E molecules on single cultured endothelial cells. When endothelial cells were co-cultured with allogeneic monocytes,expression of CD54 and CD62E were significantly up-regulated(P0.05). Conclusion It is suggested that immunoreaction between allogenic monocytes and endothelial cells leads to activation of endothelial cells,which induces expression of cell adhesion molecules and chemokines which may play a critical role in the graft rejection reaction.
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