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病毒激活的T细胞调节感染部位内皮细胞上黏附分子的表达。

Virus-activated T cells regulate expression of adhesion molecules on endothelial cells in sites of infection.

作者信息

Marker O, Scheynius A, Christensen J P, Thomsen A R

机构信息

Institute of Medical Microbiology and Immunology, University of Copenhagen, Panum Institute, Denmark.

出版信息

J Neuroimmunol. 1995 Oct;62(1):35-42. doi: 10.1016/0165-5728(95)00099-n.

Abstract

To study the role of cell adhesion molecules in the fatal CD8+ T-cell mediated meningitis which is induced by intracerebral infection with lymphocytic choriomeningitis virus, the expression of relevant molecules on inflammatory cells and local endothelium was analyzed immunohistochemically. Most inflammatory cells were strongly positive for LFA-1, VLA-4, Pgp-1 and ICAM-1. Expression of ICAM-1 and VCAM-1 was upregulated on the endothelial cells in immunocompetent mice, but not in T-cell deficient nude mice. Analysis of mice deficient in either CD4+ or CD8+ T cells, revealed that not only was the inflammatory reaction dependent on the presence of CD8+ cells, but these cells also appeared to be required for maximal upregulation of ICAM-1 and VCAM-1 on the endothelial cells. These results indicate that virus-specific CD8+ T cells are crucially involved in regulating the inflammatory reaction through effects on endothelial expression of adhesion molecules.

摘要

为研究细胞黏附分子在由淋巴细胞性脉络丛脑膜炎病毒脑内感染诱导的致死性CD8⁺T细胞介导的脑膜炎中的作用,采用免疫组织化学方法分析了炎性细胞和局部内皮细胞上相关分子的表达。大多数炎性细胞对淋巴细胞功能相关抗原-1(LFA-1)、迟现抗原-4(VLA-4)、P-糖蛋白-1(Pgp-1)和细胞间黏附分子-1(ICAM-1)呈强阳性。在免疫功能正常的小鼠中,内皮细胞上ICAM-1和血管细胞黏附分子-1(VCAM-1)的表达上调,但在T细胞缺陷的裸鼠中未上调。对CD4⁺或CD8⁺T细胞缺陷小鼠的分析表明,不仅炎症反应依赖于CD8⁺细胞的存在,而且这些细胞似乎也是内皮细胞上ICAM-1和VCAM-1最大程度上调所必需的。这些结果表明,病毒特异性CD8⁺T细胞通过影响黏附分子在内皮细胞上的表达,关键地参与调节炎症反应。

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