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作 者:刘书逊[1] 于益芝[1] 张明徽[1] 王闻雅[1] 宋文刚[2] 安华章[1] 徐红梅[1] 郭振红[1] 齐润姿[1] 曹雪涛[1]
机构地区:[1]第二军医大学免疫学研究所,上海200433 [2]泰山医学院免疫学教研室,泰安271000
出 处:《第二军医大学学报》2002年第10期1109-1113,共5页Academic Journal of Second Military Medical University
基 金:国家 973计划资助项目 (2 0 0 1CB5 10 0 0 2 ) ;国家自然科学基金资助项目 (3 9970 689) ;上海市科技启明星计划资助项目 (99QB14 0 47) ;国家 863计划资助项目 (2 0 0 1AA2 15 0 9)
摘 要:目的 :检测人单核细胞 (monocyte)和 CD34+ 干细胞来源的树突状细胞 (DC)—— Mo DC和 CD34DC,在分化发育不同阶段表达 TRAIL及 TRAIL受体 (TRAIL - Rs)的情况和外源性因子 L PS或 IFN-β刺激未成熟 DC后 TRAIL - Rs的表达变化。 方法 :采用 RT- PCR和 FACS两种方法检测人 DC表达 TRAIL和 TRAIL - Rs的水平。 结果 :人 CD34+ 干细胞在向CD34DC分化过程中 ,表达 TRAIL和 TRAIL - Rs的先后顺序为 DCR1和 DCR2 (+0 d) ,DR4和 DR5 (+5 d) ,TRAIL (+8d)。成熟 DC表达中度水平的 TRAIL、DR4、DR5、DCR2 ,不表达 DCR1。除了 DCR1外 ,Mo DC和未经诱导的单核细胞表达TRAIL及其 4个膜受体的水平基本一致 ,DCR1在诱导过程中逐渐降低。未成熟的 Mo DC在 L PS的刺激下 ,表达 DR5和 DR4的水平增高 ,在 IFN -β刺激下表达 DR5的水平增高。结论 :TRAIL和 TRAIL - Rs可能参与 DC分化或其功能的发挥。L PS或IFN-β能够增加 DC对 TRAIL诱导凋亡的敏感性 ,表明它们参与机体的免疫调控。Objective: To investigate the expression of TRAIL and TRAIL receptors on human monocyte derived dendritic cells (MoDC) and CD34 + stem cell derived dendritic cells (CD34DC) during their differentiation or after stimulated by LPS or IFN β. Methods: The expression of TRAIL and TRAIL Rs was analyzed by RT PCR and FACS. Results: During differentiation of CD34 + cells into CD34DC, cultured cells expressed DCR 1 and DCR 2 on the first day (CD34 + cells), DR4 and DR5 on the 5th day, RTAIL on the 8th day. Mature CD34DC moderately expressed TRAIL,DR4,DR5 and CDR 2, but not DCR 1. Mature MoDC and monocyte expressed TRAIL, DR4,DR5, and DCR2 at the same level. DCR 1 was expressed on monocyte, but its level decreased during differentiation of monocytes into mature MoDC. LPS stimulated immature MoDC to express DR4 and DR5, IFN β enhanced immature MoDC to express DR5. Conclusion: TRAIL and TRAIL Rs may involve in regulation of DC differentiation or its activation. LPS or IFN β may make dendritic cells prone to apoptosis through upregulation of death receptor expression, indicating that they also play important roles in regulation of immune homeostasis.
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