Gp120 activates children's brain endothelial cells via CD4

被引：0
作者：
Stins M.F. [1 ]
Shen Y. [2 ,3 ,4 ]
Huang S.H. [1 ]
Gilles F. [5 ,6 ,7 ]
Kalra V.K. [4 ,8 ,9 ]
Kim K.S. [1 ]
机构：
[1] Divisions of Infectious Diseases, USC School of Medicine, Los Angeles, CA
[2] Divisions of Biochemistry and Molecular Biology, USC School of Medicine, Los Angeles, CA
[3] Divisions of Pathology, USC School of Medicine, Los Angeles, CA
[4] Department of Pediatrics, Johns Hopkins University, School of Medicine, Baltimore, MD
[5] Childrens Hospital Los Angeles, USC School of Medicine, Los Angeles, CA
[6] Departments of Pediatrics, USC School of Medicine, Los Angeles, CA
[7] Department of Molecular Microbiology and Immunology, USC School of Medicine, Los Angeles, CA
[8] Department of Biochemistry and Molecular Biology, USC School of Medicine, Los Angeles, CA
[9] Department of Pathology, USC School of Medicine, Los Angeles, CA
来源：
Journal of NeuroVirology | 2001年 / 7卷 / 2期
关键词：
CD4; gp120; HIV-1; Human cerebral microvessel endothelium; ICAM-1; Transendothelial migration of monocytes; VCAM-1;
D O I：
10.1080/13550280152058780
中图分类号：
学科分类号：
摘要：
Encephalopathy represents a common and serious manifestation of HIV-1 infection in children, but its pathogenesis is unclear. We demonstrated that gp120 activated human brain microvascular endothelial cells (HBMEC) derived from children in up-regulating ICAM-1 and VCAM-1 expression, IL-6 secretion and increased monocyte transmigration across monolayers. Another novel observation was our demonstration of CD4 in isolated HBMEC and on microvessels of children's brain cryosections. Gp120-induced monocyte migration was inhibited by anti-gp120 and anti-CD4 antibodies. This is the first demonstration that gp120 activates HBMEC via CD4, which may contribute to the development of HIV-1 encephalopathy in children.
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页码：125 / 134
页数：9
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