HUMAN IMMUNODEFICIENCY VIRUS-INFECTED MONOCYTE-DERIVED MACROPHAGES EXPRESS SURFACE GP120 AND FUSE WITH CD4 LYMPHOID-CELLS INVITRO - A POSSIBLE MECHANISM OF LYMPHOCYTE-T DEPLETION INVIVO

被引:25
作者
CROWE, SM
MILLS, J
ELBEIK, T
LIFSON, JD
KOSEK, J
MARSHALL, JA
ENGLEMAN, EG
MCGRATH, MS
机构
[1] GENELABS INC,DIV CELLULAR IMMUNOL,REDWOOD CITY,CA 94063
[2] FAIRFIELD HOSP,MELBOURNE,VIC 3078,AUSTRALIA
[3] UNIV CALIF SAN FRANCISCO,SAN FRANCISCO GEN HOSP,DEPT MED,MED SERV,SAN FRANCISCO,CA 94110
[4] UNIV CALIF SAN FRANCISCO,SAN FRANCISCO GEN HOSP,DEPT MICROBIOL,SAN FRANCISCO,CA 94110
[5] STANFORD UNIV,MED CTR,SCH MED,DEPT PATHOL,STANFORD,CA 94305
[6] MACFARLANE BURNET CTR MED RES,MELBOURNE,VIC,AUSTRALIA
来源
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY | 1992年 / 65卷 / 02期
关键词
D O I
10.1016/0090-1229(92)90217-C
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Monocyte-derived macrophages (MDM) infected in vitro with a macrophage-tropic strain of human immunodeficiency virus (HIV) fused with uninfected, CD4-expressing T lymphoblastoid cells, but not with a subclone of these cells lacking surface CD4. Infected MDM also fused with uninfected autologous and heterologous MDM. Recombinant soluble CD4 protein (rsCD4) (10 μg/ml) and full-length recombinant glycosylated gp120 (20 μg/ml) each inhibited fusion by 94-99%; the inhibition was dose-dependent. The N-terminal portion of gp120 did not inhibit syncytium formation. Fusion was also inhibited by a monoclonal antibody to an epitope which binds gp120 (S3.5), but not by antibody to an epitope not involved in gp120 binding (OKT4). HIV-infected MDM specifically bound fluorescein-conjugated rsCD4, and virus could be visualized budding from the surface of these cells. HIV-infected MDM express viral gp120 on their surface and fuse with CD4-bearing cells in a fashion similar to lymphoid cells. Macrophages may contribute to CD4 lymphocyte depletion in vivo by this fusion mechanism. © 1992.
引用
收藏
页码:143 / 151
页数:9
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