Disruption of central nervous system barriers in multiple sclerosis

被引:246
作者
Alvarez, Jorge Ivan [1 ]
Cayrol, Romain [1 ]
Prat, Alexandre [1 ]
机构
[1] Univ Montreal, CHUM Notre Dame Hosp, Fac Med, Ctr Excellence Neur,Neuroimmunol Res Lab, Montreal, PQ H2L 4M1, Canada
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2011年 / 1812卷 / 02期
关键词
BBB; BCB; MS; EAE; CAMs; Transmigration; Neuroinflammation; Choroid plexus; Basal lamina; Basement membrane; Endothelial cells; Tight junctions; Adherens junctions; Astrocyte; Chemokine; ECM; Pericyte; ICAM-1; VCAM-1; ALCAM; VLA-4; P-selectin; Ependyma; BLOOD-BRAIN-BARRIER; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; TIGHT JUNCTION PROTEINS; INTERCELLULAR-ADHESION MOLECULE-1; MICROVASCULAR ENDOTHELIAL-CELLS; SELECTIN GLYCOPROTEIN LIGAND-1; CHEMOKINE RECEPTOR EXPRESSION; CD8(+) T-CELLS; P-SELECTIN; IN-VITRO;
D O I
10.1016/j.bbadis.2010.06.017
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The delicate microenvironment of the central nervous system (CNS) is protected by the blood-brain barrier (BBB) and the blood-cerebrospinal fluid barrier (BCB). These barriers function in distinct CNS compartments and their anatomical basis lay on the junctional proteins present in endothelial cells for the BBB and in the choroidal epithelium for the BCB. During neuroinflammatory conditions like multiple sclerosis (MS) and its murine model experimental autoimmune encephalomyelitis (EAE), activation or damage of the various cellular components of these barriers facilitate leukocyte infiltration leading to oligodendrocyte death, axonal damage, demyelination and lesion development. This manuscript will review in detail the features of these barriers under physiological and pathological conditions, particularly when focal immune activation promotes the loss of the BBB and BCB phenotype, the upregulation of cell adhesion molecules (CAMs) and the recruitment of immune cells. (C) 2010 Elsevier B.V. All rights reserved.
引用
收藏
页码:252 / 264
页数:13
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