Role of curdlan sulfate in the binding of HIV-1 gp120 to CD4 molecules and the production of gp120-mediated TNF-alpha

被引：24
|
作者：
TakedaHirokawa, N
Neoh, LP
Akimoto, H
Kaneko, H
Hishikawa, T
Sekigawa, I
Hashimoto, H
Hirose, S
Murakami, T
Yamamoto, N
Mimura, T
Kaneko, Y
机构：
[1] JUNTENDO UNIV, IZUNAGAOKA HOSP, DEPT MED, SHIZUOKA 41022, JAPAN
[2] JUNTENDO UNIV, SCH MED, DEPT RHEUMATOL & INTERNAL MED, BUNKYO KU, TOKYO 113, JAPAN
[3] AJINOMOTO CO INC, CHUO KU, TOKYO 104, JAPAN
[4] TOKYO MED & DENT UNIV, SCH MED, DEPT MICROBIOL, BUNKYO KU, TOKYO 113, JAPAN
来源：
MICROBIOLOGY AND IMMUNOLOGY | 1997年 / 41卷 / 09期
关键词：
HIV-1; gp120; curdlan sulfate; TNF-alpha;
D O I：
10.1111/j.1348-0421.1997.tb01920.x
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
To clarify the mechanism by which curdlan sulfate (CRDS) inhibits human immunodeficiency virus (HIV)-1 infection, we examined its influence on the binding of gp120 to CD4 molecules on T cells and macrophages, as well as on the production of TNF-alpha by gp120-stimulated macrophages (which promotes HIV-1 replication). CRDS treatment of cells not only inhibited the binding of HIV-1 gp120 to CD4(+) cells, but also inhibited TNF-alpha production induced by gp120. Inhibition of HIV-1 infection by CRDS may be related to these two actions.
引用
收藏
页码：741 / 745
页数：5
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