检索结果-南通市图书馆

第八届全国免疫学学术大会

作者： Chunyan Yu Zhengle tang Christian Bronner Xijian Lu Jingfang Di Shan Zeng Jing Liu Feiyue Xing Institute of tissue transplantation and Immunology Department of ImmunobiologyJinan University

Background:Recent studies have shown that anisomycin significantly inhibits mammalian cell proliferation, but its mechanism remains *** this study, jurkat t cells were used to first explore a relationship between effect of anisomycin on them and alteration of cell cycle-regulating ***:cell colony formation, CCK-8 assay, Flow cytometry, Rt-PCR and Western blot were employed to evaluate correlation of ten cell cycle-regulating proteins with suppression of the cell proliferation and arrest of the cell cycle by ***:Our data showed that anisomycin inhibited the colony-formation and proliferation of jurkat t cells in a dose-dependent manner, and arrested the cells into S and G2/M phases with the production of sub-diploid *** levels of P21, P-P27 and P53/P-P53 reached to their peaks 4 h after anisomycin treatment, presenting a positive correlation with anisomycin concentration, and P16, P-P21, P27, P57, P73/P-P73 and P- Rb changed little with the exposure time or concentrations of *** the level of Rb protein was increased at 24 h after the treatment of *** expression of an inverted CCAAt box binding protein(ICBP90) in jurkat t cells came to decrease 12 h after the treatment of anisomycin, presenting a negative correlation with anisomycin ***, the expression of P-CDK2 was also decreased at 24 h, presenting an obviously negative correlation, whereas P-CDK1 showed no differences among the differently treated jurkat t ***, the level of P21 and P53 mRNA was increased with the enhanced concentrations of ***:the results indicate that anisomycin may mainly activate the P53/P21 signaling to decrease the expression of ICBP90, inhibit expression of P-CDK2 to block the cells into S and G2/M phases, and finally result in proliferation inhibition of jurkat t cells.

关键词： Anisomycin P21 P53 ICBP90 CDK2 jurkat t cell

来源： cnki会议评论

在线全文

cnki会议

学校读者我要写书评

暂无评论

Inhibition of the α-mannosidase Man2c1 gene expression enhances adhesion of jurkat cells

引用

cell Research 2006年第7期16卷 622-631页

作者： Li Qu~(1,*) Ji Yu Ju~(1,*) Shuang Ling Chen~1 Yan Shi~1 Zhi Guang Xiang~1 Yi Qun Zhou~1 Yun tian~1 Yin Liu~1 Li Ping Zhu~1 ~1Department of Immunology,Institute of Basic Medical Sciences,Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing 100005,China DepartmentofImmunology InstituteofBasicMedicalSciencesChineseAcademyofMedicalSciencesandPekingUnionMedicalCollegeBeijing100005China

Protein N-glycosylation plays very important roles in immunity and α-mannosidase is one of the key enzymes in *** paper reports that inhibition of α-mannosidase Man2cl gene expression enhances adhesion of jurkatt *** comparison to the controls with normal expression of the enzyme,jurkat cells with the inhibition of Man2clgene expression（AS cell）formed larger aggregates in culture,indicating an enhancement of adhesion between the *** differential display analysis discovered up-regulation of several adhesion molecule genes in the AS *** the pivotal role played by CD54-LFA-1 interaction in immune cell interaction,this study focused on the contributionof enhanced expression of CD54 and LFA-1 to the enhanced adhesion of AS jurkat *** facts,including increasedbinding of AS cells to ICAM-1-Fc,Mg2+activation of the binding of AS cells to ICAM-1-Fc and enhanced aggregationof AS cells,together with the inhibiting effect of a blocking CD 11a mAb on the binding to ICAM-1-Fc and aggregationof the cells demonstrate an important contribution of enhanced CD54-LFA-1 interaction to increased adhesion betweenAS *** enhanced CD54-LFA-1 interaction also resulted in increased adhesion between AS jurkat t cells and RajiB *** addition,AS cells showed cytoskeletal *** data imply a biological significance of MAN2C1in t-cell functioning.

关键词： Man2cl jurkat t cell adhesion CD54-LFA-1 cytoskeleton

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

靶向MUC1嵌合抗原受体修饰的jurkat t细胞杀伤肝癌细胞的研究

靶向MUC1嵌合抗原受体修饰的Jurkat T细胞杀伤肝癌细胞的研究

引用

作者：马宜冬苏州大学

学位级别：硕士

嵌合抗原受体（chimeric antigen receptor，CAR）由一个scFv(single chain variablefragment)单链抗体可变区片段（由抗体VH氨基酸序列和VL区氨基酸序列经Linker连接而成），通过铰链结构与源于tCR复合体或者IgE高亲和受体的跨膜和胞... 详细信息

嵌合抗原受体（chimeric antigen receptor，CAR）由一个scFv(single chain variablefragment)单链抗体可变区片段（由抗体VH氨基酸序列和VL区氨基酸序列经Linker连接而成），通过铰链结构与源于tCR复合体或者IgE高亲和受体的跨膜和胞内信号结构域（源CD3ζ/FcεRIγ免疫受体酪氨酸活化基序、源自CD28/4-1BB/OX40/ICOS/DAP10/LCK共刺激信号分子胞内结构域）连接构成。经CAR遗传修饰的t细胞（简称CAR-t），能够高效识别和杀伤由于MHC分子或抗原加工相关蛋白酶体低表达、逃逸tCR介导免疫反应的肿瘤细胞。 MUC1（Mucin1，黏蛋白1）是一种大分子跨膜糖蛋白，广泛高表达于乳腺癌、卵巢癌、肺癌、前列腺癌、结肠癌、肝癌和胰腺癌等恶性肿瘤，它的胞外区主要由20个氨基酸（PDtRPAPGStAPPAHGVtSA）的核心重复序列组成，是MUC1蛋白糖基化修饰位点，且相对于正常细胞，肿瘤细胞表面MUC1具有不同的糖基化结构。过表达和糖基化异常都使MUC1成为各种免疫治疗的理想靶点。本课题中我们以MUC1作为免疫靶点，分别构建第一代与第三代靶向MUC1的CAR基因表达框（MUC1-CAR和G3MUC1-CAR），并将其装入慢病毒载体，利用获得的重组慢病毒感染jurkat细胞，通过CCK-8法、ELISA法、乳酸脱氢酶释放实验，分别检测在MUC1抗原存在条件下，CAR-t细胞的增殖、IL-2分泌量、杀伤作用。实验中我们成功构建两种靶向MUC1嵌合抗原受体表达框、重组慢病毒、jurkat CAR-t细胞株。两种经MUC1嵌合抗原受体修饰的jurkat CAR-t细胞均能特异识别MUC1分子，杀伤MUC1高表达的肝癌细胞QGY-7701，而对MUC1低表达的正常肝细胞L02基本不杀伤;相对于第一代CAR，第三代CAR修饰的jurkatt细胞接触MUC1分子后，其增殖速度、IL-2分泌量和杀伤效率均显著优于第一代MUC1修饰细胞（MUC1-CAR）。本课题研究结果表明：靶向MUC1的jurkat CAR-t细胞能特异杀伤MUC1高表达的肝癌细胞，为应用MUC1-CAR修饰的患者原代t细胞用于肝癌过继性免疫细胞治疗的研究提供了可靠实验依据。

关键词：嵌合抗原受体 MUC1 jurkat t cell 肝癌细胞

来源：

同方学位论文库评论

在线全文

同方学位论文库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：