The adhesion molecule ICAM-1 and its regulation in relation with the blood-brain barrier

被引:210
作者
Dietrich, JB [1 ]
机构
[1] INSERM, U338, F-67084 Strasbourg, France
关键词
blood-brain barrier; endothelial cells; intercellular adhesion molecule 1; regulation;
D O I
10.1016/S0165-5728(02)00114-5
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The blood-brain barrier (BBB) is formed by high resistance tight junctions within the capillary endothelium perfusing the vertebrate brain. Normal BBB maintains a unique microenvironment within the central nervous system (CNS). In neurodegenerative disorders (for example multiple sclerosis, MS), the BBB becomes impaired. Perivascular cells (astrocytes, macrophages and microglial cells) and brain microvascular endothelial cells (BMEC) produce various inflammatory factors that affect the BBB permeability and the expression of adhesion molecules. Indeed, cytokines can stimulate the expression of several adhesion molecules on brain microvascular endothelial cells. Among these adhesion molecules, the intercellular adhesion molecule-1 (ICAM-1) binds to its leukocyte ligands and allows activated leukocytes entry into the CNS. This review is dealing with the expression and regulation of ICAM-1 in relation with several properties of the BBB. Particularly, the role of ICAM-1 in the control of the leukocyte traffic into the CNS, as well as in cerebral malaria and in CNS infection by viruses, is discussed. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:58 / 68
页数:11
相关论文
共 120 条
[1]   Differential binding of clonal variants of Plasmodium falciparum to allelic forms of intracellular adhesion molecule 1 determined by flow adhesion assay [J].
Adams, S ;
Turner, GDH ;
Nash, GB ;
Micklem, K ;
Newbold, CI ;
Craig, AG .
INFECTION AND IMMUNITY, 2000, 68 (01) :264-269
[2]  
Adamson P, 1999, J IMMUNOL, V162, P2964
[3]   REGULATION OF INTERCELLULAR-ADHESION MOLECULE-1 EXPRESSION BY RETINOIC ACID - ANALYSIS OF THE 5' REGULATORY REGION OF THE GENE [J].
AOUDJIT, F ;
BOSSE, M ;
STRATOWA, C ;
VORABERGER, G ;
AUDETTE, M .
INTERNATIONAL JOURNAL OF CANCER, 1994, 58 (04) :543-549
[4]  
Aoudjit F, 1998, J IMMUNOL, V160, P2967
[5]   Insulin like growth factor-1 activates nuclear factor-κB and increases transcription of the intercellular adhesion molecule-1 gene in endothelial cells [J].
Balaram, SK ;
Agarwal, DK ;
Edwards, JD .
CARDIOVASCULAR SURGERY, 1999, 7 (01) :91-97
[6]   Signal transduction by tumor necrosis factor and its relatives [J].
Baud, V ;
Karin, M .
TRENDS IN CELL BIOLOGY, 2001, 11 (09) :372-377
[7]   Cellular responses to interferon-gamma [J].
Boehm, U ;
Klamp, T ;
Groot, M ;
Howard, JC .
ANNUAL REVIEW OF IMMUNOLOGY, 1997, 15 :749-795
[8]   Loss of the tight junction proteins occludin and zonula occludens-1 from cerebral vascular endothelium during neutrophil-induced blood-brain barrier breakdown in vivo [J].
Bolton, SJ ;
Anthony, DC ;
Perry, VH .
NEUROSCIENCE, 1998, 86 (04) :1245-1257
[9]   Presence of host ICAM-1 in laboratory and clinical strains of human immunodeficiency virus type 1 increases virus infectivity and CD4+-T-cell depletion in human lymphoid tissue, a major site of replication in vivo [J].
Bounou, S ;
Leclerc, JE ;
Tremblay, MJ .
JOURNAL OF VIROLOGY, 2002, 76 (03) :1004-1014
[10]  
Bourke E, 1999, J IMMUNOL, V163, P2113