HERPES-SIMPLEX VIRUS TYPE-1 FC RECEPTOR PROTECTS INFECTED-CELLS FROM ANTIBODY-DEPENDENT CELLULAR CYTOTOXICITY

被引：123
|
作者：
DUBIN, G
SOCOLOF, E
FRANK, I
FRIEDMAN, HM
机构：
[1] UNIV PENN,DEPT MED,INFECT DIS SECT,PHILADELPHIA,PA 19104
[2] CHILDRENS HOSP PHILADELPHIA,DEPT PATHOL & LAB MED,PHILADELPHIA,PA 19104
来源：
JOURNAL OF VIROLOGY | 1991年 / 65卷 / 12期
关键词：
D O I：
10.1128/JVI.65.12.7046-7050.1991
中图分类号：
Q93 [微生物学];
学科分类号：
071005 ; 100705 ;
摘要：
Recent studies indicate that the herpes simplex virus type 1 (HSV-1) Fc receptor (FcR) can bind antiviral immunoglobulin G by participating in antibody bipolar bridging. This occurs when the Fab domain of an immunoglobulin G molecule binds to its antigenic target and the Fc domain binds to the HSV-1 FcR. In experiments comparing cells infected with wild-type HSV-1 (NS) and cells infected with an FcR-deficient mutant (ENS), we demonstrate that participation of the HSV-1 FcR in antibody bipolar bridging reduces the effectiveness of antibody-dependent cellular cytotoxicity.
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页码：7046 / 7050
页数：5
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