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作 者:向晓星[1] 周霞秋[1] 王俊学[2] 谢青[1] 蔡雄[2] 俞红[1] 周惠娟[1]
机构地区:[1]上海第二医科大学瑞金医院感染科,上海200025 [2]第二军医大学长征医院感染科,上海200003
出 处:《基础医学与临床》2006年第6期597-601,共5页Basic and Clinical Medicine
基 金:上海市科委科研计划项目(044119624)
摘 要:目的研究CpG寡核苷酸(CpG-ODN)对慢性乙肝患者(CHB)外周血树突细胞(DC)表型和功能、细胞因子信号传导分子(STAT)及其抑制因子(SOCS)表达的影响。方法以细胞因子GM-CSF、IL-4自CHB和健康者外周血单核细胞诱导扩增DC,以CpG-ODN或TNF-α刺激DC,评价其对DC表型和功能的影响;应用W estern印迹法检测DC胞质STAT1、3、4、5、6以及SOCS1、3蛋白的表达。结果TNF-α、CpG-ODN能明显增强CHB患者DC的HLA-DR和IL-12 p70表达以及T细胞促增殖能力,但不能增强CD1 a的表达;两者能不同程度增强DC胞质STAT1、4、6和SOCS1、3的表达,但不影响STAT3、5的表达。结论CpG-ODN与TNF-α一样可能通过调节DC胞质信号分子STAT1、4、6及SOCS1、3的表达促进CHB外周血DC分化、成熟及其抗原递呈功能。Objective To study the effect of CpG containing oligodeoxynucleotide (CpG-ODN) on the phenotypes, function and expression of signal transductors and activators of transcription (STAT) and suppressors of cell signaling(SOCS) of peripheral blood dendritic cells(DC) in patients with chronic hepatitis B (CHB). Methods Mono- cytes isolated from peripheral blood of CHB and healthy volunteers were cultured and induced by granulocyte-monocyte colony stimulating factor(GM-CSF) and interleukin-4 (IL-4). Then, CpG-ODN or TNF-α were added to stimulate the immatured DC, their effects on the phenotypes and function of DC were evaluated. The expression of signaling molecules of STAT1, 3, 4, 5, 6 and SOCS1, 3 in DC were detected by Western blotting. Results The expression rates of HLA-DR of DC in CHB with the treatment of CpG-ODN or TNF-α were obviously increased; Both the IL-12p70 expression and stimulating capacity of DC to allogenic T lymphocytes were improved significantly in CpG-ODN group and TNF-ot group(P 〈0. 01 and 0.05, respectively) ; However neither CpG-ODN nor TNF-α could improve the expression of CDla. Both CpG-ODN and TNF-α enhanced the expression of intracellular STAT1,4, 6 and SOCS1, 3 in DC of CHB, but not affect the expression of STAT3, 5. Conclusions CpG-ODN,like TNF-α, has remarkable stimulatory effect on the impaired phenotype and function of peripheral blood DC in patients with chronic hepatitis B and the mechanism is potentially explained by regulating the expression of signal molecules of STAT1,4, 6 and SOCS1, 3 in DC.
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