Alvarez Jorge Ivan, Cayrol Romain, Prat Alexandre
Neuroimmunology Research Laboratory, Center of Excellence in Neuromics, CHUM-Notre-Dame Hospital, Faculty of Medicine, Université de Montréal, Montréal, Québec, Canada.
Biochim Biophys Acta. 2011 Feb;1812(2):252-64. doi: 10.1016/j.bbadis.2010.06.017. Epub 2010 Jul 7.
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.
中枢神经系统（CNS）的微妙微环境由血脑屏障（BBB）和血脑脊液屏障（BCB）保护。这些屏障在不同的CNS区域发挥作用，其解剖学基础在于BBB的内皮细胞和BCB的脉络丛上皮细胞中存在的连接蛋白。在诸如多发性硬化症（MS）及其小鼠模型实验性自身免疫性脑脊髓炎（EAE）等神经炎症性疾病中，这些屏障的各种细胞成分的激活或损伤会促进白细胞浸润，导致少突胶质细胞死亡、轴突损伤、脱髓鞘和病变发展。本手稿将详细综述这些屏障在生理和病理条件下的特征，特别是当局部免疫激活促进BBB和BCB表型丧失、细胞粘附分子（CAMs）上调以及免疫细胞募集时的情况。
