期刊
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
卷 62, 期 4, 页码 412-419出版社
AMER ASSN NEUROPATHOLOGISTS INC
DOI: 10.1093/jnen/62.4.412
关键词
adhesion molecules; chemokines; endothelial cells; human; migration; monocyte
We hake used human brain-derived endothelial cells (HBECs) maintained under basal culture conditions in a Boyden chamber assay system as an in vitro model of migration of cells of systemic immune origin across the blood brain barrier (BBB) during the initiation of a CNS-directed inflammatory reponse. In this study we evaluated the molecular mechanisms that regulate passage of ex vivo peripheral blood-derived monocytes across this barrier and the effects of such migration on the properties of both the HBECs and the monocytes. Our results indicate that monocytes can migrate across HBECs in the absence of inflammatory conditions, at rates exceeding those of lymphocytes. Monocyte migration could be significantly inhibited by the addition of blocking antibodies to intercellular adhesion molecule (ICAM)-1, very late antigen (VLA)-4 integrin, and monocyte chemoattractant protein (CCL-2/MCP-1), or treatment with tissue inhibitor of metalloproteinase (TIMP-1). Following monocyte migration there was a significant increase in permeability of soluble molecules and an enhanced rate of T cell migration across HBECs. The enhanced permeability could he partially presented with anti-TNF-alpha antibody. The migration process did not induce the upregulation of either co-stimulatory molecules or chemokine receptors on the monocytes. These studies emphasize the functional role of monocyte-endothelial interactions in permitting target access of a CNS-directed cell-mediated immune response.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据