FADDdel-GFP-Modified Mouse Insulinoma Cells Counteract the Cytotoxicity of Reactive T Cells  

作　　者：PingHu GuohuaWang XiaohuaZhu JingYang HuifenZhu ZihuiXu WenjunLiao XiaoLiu FenXu JiaoYin GuanxinShen 

机构地区：[1]DepartmentofImmunology,TongjiMedicalCollegeofHuazhongUniversityofScienceandTechnology,Wuhan430030,China. [2]InstituteofBiochemistryandMolecularBiology,HubeiUniversity,Wuhan430062,China. [3]DepartmentofPathogenicBiology,TongjiMedicalCollegeofHuazhongUniversityofScienceandTechnology,Wuhan430030,China.

出　　处：《Cellular & Molecular Immunology》2004年第5期383-386,共4页中国免疫学杂志（英文版）

基　　金：This study was supported by National Key Basic Research Program of China(No.CB5 10008);National Natural Science foundation(No.30300166).

摘　　要：IDDM results from pancreatic beta cell destruction by islet-reactive T cells,a process that involves beta cell apoptosis.Fas-FasL pathway plays a major role in pancreatic β cell death.Fas-associated death domain protein (FADD),the component of the tumor necrosis factor receptor type 1(TNFR1) and Fas signaling complexes,is involved in TNFR1-and Fas-induced apoptosis.Inhibiting the function of FADD will lead to blocking downstream apoptosis signal,which protects pancreatic β cells from destruction by Fas-FasL pathway.In this study we constructed eukaryotic expressing vector of fusional protein FADDdel-GFP named pFADDdel-GFP. After pFADDdel-GFP was transfected into NIT,the expression of FADDdel-GFP in NIT was detected by fluorescence microscopy and the resistance of NIT transfected with pFADDdel-GFP to cytotoxicity mediated by special T cells was detected by FACS and MTT.The results showed that NIT modified by pFADDdel-GFP obviously resisted cytotoxicity mediated by special T cells.Therefore,it may be useful in the prevention or treatment of IDDM by intervening Fas-FasL pathway.Cellular & Molecular Immunology.2004;1(5):383-386.IDDM results from pancreatic beta cell destruction by islet-reactive T cells,a process that involves beta cell apoptosis.Fas-FasL pathway plays a major role in pancreatic β cell death.Fas-associated death domain protein (FADD),the component of the tumor necrosis factor receptor type 1(TNFR1) and Fas signaling complexes,is involved in TNFR1-and Fas-induced apoptosis.Inhibiting the function of FADD will lead to blocking downstream apoptosis signal,which protects pancreatic β cells from destruction by Fas-FasL pathway.In this study we constructed eukaryotic expressing vector of fusional protein FADDdel-GFP named pFADDdel-GFP. After pFADDdel-GFP was transfected into NIT,the expression of FADDdel-GFP in NIT was detected by fluorescence microscopy and the resistance of NIT transfected with pFADDdel-GFP to cytotoxicity mediated by special T cells was detected by FACS and MTT.The results showed that NIT modified by pFADDdel-GFP obviously resisted cytotoxicity mediated by special T cells.Therefore,it may be useful in the prevention or treatment of IDDM by intervening Fas-FasL pathway.Cellular & Molecular Immunology.2004;1(5):383-386.

关 键 词：FADD NIT TRANSDUCTION 

分 类 号：R736.7[医药卫生—肿瘤]