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

页码：741 / 745

页数：5

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