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儿茶酚胺刺激牛脑毛细血管内皮细胞上由γ-干扰素诱导的II类主要组织相容性复合体的表达。

Catecholamines stimulate the IFN-gamma-induced class II MHC expression on bovine brain capillary endothelial cells.

作者信息

Coutinho G C, Durieu-Trautmann O, Strosberg A D, Couraud P O

机构信息

Laboratoire d'Immuno-Pharmacologie Moléculaire, UPR 0415 CNRS, Paris, France.

出版信息

J Immunol. 1991 Oct 15;147(8):2525-9.

PMID:1717565
Abstract

The brain has been considered for a long time as an immunologically privileged site because of the lack of a true lymphatic system and the existence of several barriers that isolate it from the periphery. In the last few years, it became evident that cells in the central nervous system (astrocytes, microglial cells, and brain capillary endothelial cells) can be induced to express class II MHC and present Ag to T lymphocytes. The brain capillary endothelial cells, which are strategically located at the interface between blood and brain, could be involved in the initiation of immune responses within the brain parenchyma. We have previously characterized bovine brain capillary endothelial cells in culture and shown that they maintain in vitro a fully differentiated phenotype associated with the blood-brain barrier endothelium. In order to assess the role of these cells in the development of immune responses in the brain, we initiated the present study on the regulation of their class II MHC surface expression. Our data indicate that this expression on bovine brain capillary endothelial cells is inducible by IFN-gamma and further stimulated by catecholamines through activation of beta-adrenergic receptors. However, this latter effect is not mimicked by forskolin, theophylline, or dibutyryl-cAMP, suggesting the involvement of a cAMP-independent mechanism.

摘要

长期以来,由于缺乏真正的淋巴系统以及存在将其与外周隔离的多种屏障,大脑一直被视为免疫特惠部位。在过去几年中,有一点变得很明显,即中枢神经系统中的细胞(星形胶质细胞、小胶质细胞和脑毛细血管内皮细胞)可被诱导表达II类主要组织相容性复合体(MHC)并将抗原呈递给T淋巴细胞。战略性地位于血液与大脑界面的脑毛细血管内皮细胞,可能参与脑实质内免疫反应的启动。我们之前已对培养的牛脑毛细血管内皮细胞进行了表征,并表明它们在体外维持与血脑屏障内皮相关的完全分化表型。为了评估这些细胞在大脑免疫反应发展中的作用,我们启动了本研究,以探讨其II类MHC表面表达的调控机制。我们的数据表明,牛脑毛细血管内皮细胞上的这种表达可被γ干扰素诱导,并通过β-肾上腺素能受体的激活进一步受到儿茶酚胺的刺激。然而,福斯可林、茶碱或二丁酰环磷腺苷不能模拟后一种效应,这表明涉及一种不依赖环磷腺苷的机制。

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