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2型单纯疱疹病毒感染小鼠脑内细胞因子产生、黏附分子诱导及T细胞募集缺陷的证据。

Evidence for deficiencies in intracerebral cytokine production, adhesion molecule induction, and T cell recruitment in herpes simplex virus type-2 infected mice.

作者信息

Lewandowski G, Hobbs M V

机构信息

Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA 92037, USA.

出版信息

J Neuroimmunol. 1998 Jan;81(1-2):58-65. doi: 10.1016/s0165-5728(97)00159-8.

Abstract

We examined the intracerebral T cell response in mice infected with neurovirulent HSV-2 strains and an avirulent HSV-1. In HSV-2-infected brains, (i) IL-1beta, TNF-alpha and IFN-gamma mRNA expression was low, (ii) ICAM-1 and VCAM-1 were not induced, (iii) few CD4+ or CD8+ cells were detected. By contrast, in HSV-1-infected brains, (i) cytokine mRNA expression was high, (ii) adhesion molecules were strongly expressed, (iii) many T cells were detected. We suggest that deficient T cell extravasation into HSV-2-infected brain regions is caused by negligible ICAM-1 and VCAM-1 expression, which is due to low expression of critical cytokines.

摘要

我们检测了感染神经毒性HSV-2毒株和无毒力HSV-1的小鼠的小鼠脑内的T细胞反应。在感染HSV-2的脑中,(i)白细胞介素-1β、肿瘤坏死因子-α和干扰素-γ的mRNA表达水平较低,(ii)细胞间黏附分子-1(ICAM-1)和血管细胞黏附分子-1(VCAM-1)未被诱导表达,(iii)检测到的CD4+或CD8+细胞很少。相比之下,在感染HSV-1的脑中,(i)细胞因子mRNA表达水平较高,(ii)黏附分子强烈表达,(iii)检测到许多T细胞。我们认为,T细胞向HSV-2感染脑区的渗出不足是由于ICAM-1和VCAM-1表达可忽略不计所致,而这又是关键细胞因子表达水平较低的结果。

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