STABLE EXPRESSION AND FUNCTION OF EBV/C3D RECEPTOR FOLLOWING GENOMIC TRANSFECTION INTO MURINE FIBROBLAST L-CELLS

被引:9
作者
CANTALOUBE, JF
PIECHACZYK, M
CALENDER, A
LENOIR, G
MINTY, A
CARRIERE, D
FISCHER, E
PONCELET, P
机构
[1] SANOFI RECH,SERV IMMUNOL,MONTPELLIER,FRANCE
[2] UNIV MONTPELLIER 2,BIOL MOLEC LAB,F-34060 MONTPELLIER,FRANCE
[3] CTR INT RECH CANC,LYONS,FRANCE
[4] SANOFI ELF BIO RECH,LABEGE,FRANCE
[5] HOP BROUSSAIS,INSERM,U28,F-75674 PARIS 14,FRANCE
关键词
D O I
10.1002/eji.1830200226
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The Epstein‐Barr virus (EBV) and the C3d component of complement bind to the same cell surface receptor (EBVR/CR2) which is part of the B lymphocyte differentiation antigen recognized by the monoclonal antibodies (mAb) of the cluster of differentiation 21 (CD21). To analyze EBV and C3d binding to this receptor, mouse fibroblasts were transfected with human genomic DNA and rare CD21‐positive cells were selected and cloned by cell sorting. The presence of the human gene in host cell DNA as well as its transcription product were assayed with a cloned EBVR/CR2 cDNA by Southern and Northern blotting analysis, respectively. A glycoprotein of apparent molecular mass of 140 kDa, similar to that found in human B lymphocytes, was immunoprecipitated with anti‐CD21 mAb and proved to be functional since both C3d and EBV bound efficiently and specifically to mouse cells expressing EBVR/CR2. However, no expression of EBV nuclear antigens, early antigens and viral capsid antigens was detected in cells exposed to EBV. This indicates that the presence of EBVR/CR2 is not sufficient to allow full infection of mouse fibroblasts. Copyright © 1990 Wiley‐VCH Verlag GmbH & Co. KGaA, Weinheim
引用
收藏
页码:409 / 416
页数:8
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