Silencing invariant chain of DCs enhances Th1 response using small interfering RNA  

作　　者：柯山 陈雪华 黎皓 朱正纲 

机构地区：[1]Department of Surgery,Shanghai Institute of Digestive Surgery,Ruijin Hospital,School of Medicine,Shanghai Jiaotong University

出　　处：《上海交通大学学报（医学版）》2007年第5期502-502,共1页Journal of Shanghai Jiao tong University:Medical Science

基　　金：National Nature Science Foundation of China(30570828,30471961,30170915).

摘　　要：RNA interference(RNAi),which causes the degradation of any RNA in a sequence specific manner,is a posttranscriptional gene silencing mechanism.Targeting the invariant chain(Ii)in DCs has been used as an approach to enhance antitumor immunity.It is demonstrated in this article that transfection of H-2(K)DCs with siRNA specific for Ii gene can significantly knock down Ii.When exposed to TNF-alpha,immature DCs transfected with Ii siRNA can differentiate into mature DCs without reducing viability or IL-12p70 production.Ii siRNA-treated H-2(K)DCs exhibited an increased allostimulatory capacity in a lymphocyte proliferation assay.Furthermore,Ii siRNA-transfected H-2(K)DCs enhanced Th1 responses by increasing IFN-gamma and decreasing IL-4 production,and much stronger cytotoxic activity was observed when DCs were co-transfected with Ii siRNA and an endogenous tumor antigen in vitro.Our findings indicate that silencing the Ii gene in DCs with siRNA may offer a potential approach to enhancing antitumor immunotherapy.RNA interference （RNAi） , which causes the degradation of any RNA in a sequence specific manner, is a posttranscriptional gene silencing mechanism. Targeting the invariant chain （li） in DCs has been used as an approach to enhance antitumor immunity. It is demon- strated in this article that transfection of H-2（K） DCs with siRNA specific for li gene can significantly knock down li. When exposed to TNF-alpha, immature DCs transfected with li siRNA can differentiate into mature DCs without reducing viability or IL-12p70 production.

关 键 词：RNA干涉 抗癌活性 免疫 抗原提呈细胞 H-2(K) 转染 基因沉默 

分 类 号：Q78[生物学—分子生物学] R392.2[医药卫生—免疫学]