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荧光素酶表达的淋巴瘤NCG小鼠模型的构建

The Establishment of Luciferase-expressing Lymphoma Model in NCG Mice
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摘要 目前建立的淋巴瘤动物模型大多是通过裸鼠皮下注射淋巴瘤细胞得到的,通过游标卡尺测量肿瘤大小,存在测量数据误差大,不能发现微小病灶,小鼠模型不适应于评估嵌合抗原受体T细胞(CAR-T)疗法等问题.本研究旨在通过慢病毒载体导入荧光素酶基因,经嘌呤霉素筛选得到稳定表达荧光素酶的Raji细胞(Raji-luc+),细胞生物发光强度与细胞数量成正比,NOD-Prkdcem26Cd52Il2rgem26Cd22/Nju(NCG)免疫缺陷小鼠尾静脉注射Raji-luc+(1×106)细胞,通过活体成像仪连续检测,发现注射Raji-luc+细胞后发光强度逐渐增强,意味着淋巴瘤细胞在小鼠体内逐渐增殖和扩散,并建立生存曲线.这些数据表明成功建立了荧光素酶标记的淋巴瘤小鼠模型. At present,animal models of lymphoma are mostly established by subcutaneous injection lymphoma cells in nude mice.The evaluation of these models remains limitation,as the tumor size is roughly measured by a vernier caliper and the tiny lesions can not be intensively detected.These current models are hence not suitable for evaluating CAR-T therapy.The purpose of this study was to import luciferase gene by lentiviral vector for first getting puromycin-selected,luciferase-stably-expressing Raji-luc +cells,And the cells characteristics were monitored as the luminous intensity of cells was proportional to the number of cells,then these generated Raji-luc+ cells(1×106)was injected into NCG mice via,the tail vein,continuous detection by in vivo imaging devices revealed that the luminescence intensity was gradually increased after Raji-luc+ cells transplantation,indicating the growth and spread of lymphoma cells in vivo.The mice survival cure was then established in this study.These data suggest that the luciferase-expressing lymphoma model in NCG mice is established.
作者 钟杨城 陆盼盼 王亚楠 姜正涛 杨辛毅 杨鹤 潘含雨 赵琳 李博康 周牧涯 朱焕章 ZHONG Yangcheng;LU Panpan;WANG Yanan;JIANG Zhengtao;YANG Xinyi;YANG He;PAN Hanyu;ZHAO Lin;LI Bokang;ZHOU Muya;ZHU Huanzhang(School of Life Sciences,Fudan University,Shanghai 200438,China;State Key Laboratory of Genetic Engineering,Fudan University,Shanghai 200438,China)
出处 《复旦学报(自然科学版)》 CAS CSCD 北大核心 2018年第6期725-731,共7页 Journal of Fudan University:Natural Science
基金 "十三五"国家科技重大专项(2017ZX1020202102-002)
关键词 淋巴瘤 RAJI细胞 荧光素酶 活体成像 NCG 嵌合抗原受体T细胞 Lymphoma Raji cells Luciferase Live imaging NCG CAR-T
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  • 1Davey R T, Bhat N, Yoder C, et al. HIV-1 and T cell dynamics after interruption of highly active antiretroviral therapy (HAART) in patients with a history of sustained viral suppression[J]. Proc Natl Acad Sci USA, 1999, 96(26) : 15109-15114.
  • 2Persaucl D, Zhou Y, Siliciano J M, et al. Latency in human immunodeficiency virus type 1 infection: No easy answers[J]. Journal of Virology, 2003, 77(3) : 1659-1665.
  • 3Han Y F, Wind-Rotolo M, Yang H C, et al. Experimental approaches to the study of HIV-1 latency[J]. Nature Reviews Microbiology, 2007, 5: 95-106.
  • 4Williams S A, Greene W C. Regulation of HIV-1 latency by T-cell activation[J]. Cytokine, 2007, 39(1) : 63-74.
  • 5Riehman D D, Margolis D M, Delaney M, et al. The challenge of finding a cure for HIV infection[J]. Science, 2009, 323(5919) : 1304-1307.
  • 6Colin I.,Van I.int C. Molecular control of HIV-1 postintegration latency: implications for the development of new therapeutic strategies[J]. Retrovirology, 2009, 6: 111.
  • 7Chun T W, Carruth L, Finzi D, et al. Quantification of latent tissue reservoirs and total body viral load in HIV-1 Infection[J]. Nature, 1997, 387(6629).. 183-188.
  • 8Coiras M, Lopez-Huertas M R, Perez-Olmeda M, et al. Understanding HIV-1 latency provides clues for the eradication of long-term reservoirs[J]. Nature Reviews Microbiology, 2009, 7(11): 798-812.
  • 9Quivy V, De Walque S, Van Lint C. Chromatin-associated regulation of HIV-1 transcription: implications for the development of therapeutic strategies[J]. Subcell Biochem, 2007, 41: 371-96.
  • 10Williams S A, Chen L F, Kwon H, et al. Prostratin antagonizes HIV latency by activating NF-kappaB [J]. J Biol Chem, 2004, 279(40): 42008-17.

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