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自然杀伤细胞和TCRγδ T细胞在急性自身免疫性脑脊髓炎中的作用。

Role of natural killer cells and TCR gamma delta T cells in acute autoimmune encephalomyelitis.

作者信息

Matsumoto Y, Kohyama K, Aikawa Y, Shin T, Kawazoe Y, Suzuki Y, Tanuma N

机构信息

Department of Neuropathology, Tokyo Metropolitan Institute for Neuroscience, Fuchu City, Japan.

出版信息

Eur J Immunol. 1998 May;28(5):1681-8. doi: 10.1002/(SICI)1521-4141(199805)28:05<1681::AID-IMMU1681>3.0.CO;2-T.

DOI:10.1002/(SICI)1521-4141(199805)28:05<1681::AID-IMMU1681>3.0.CO;2-T
PMID:9603475
Abstract

To elucidate the role of NK cells and TCR gamma delta+ T cells in acute experimental autoimmune encephalomyelitis (EAE) induced in Lewis rats, the distribution, number and function of these cells were studied using several methods. Immunohistochemical and flow cytometric analysis revealed that a certain number of NK cells (17 of the total inflammatory cells) infiltrated the central nervous system (CNS) at the peak stage of EAE and were mainly located in the perivascular region. On the other hand, virtually no TCR gamma delta+ T cells were found in the CNS. NK-T (NKR-P1+TCR alpha beta+) cells were few and did not increase in number in the CNS and lymphoid organs. In the cytotoxic assay using YAC-1 cells, effector cells isolated from the spleen of rats at the peak of EAE showed essentially the same cytotoxicity as those isolated from normal controls although the total number of NK cells decreased to one fifth of that of normal rats. Furthermore, in vivo administration of anti-NK cell (3.2.3 and anti-asialo GM1), but not of anti-TCR gamma delta (V65), antibodies exacerbated the clinical features of EAE and induced fatal EAE in some rats. These findings suggest that NK cells play a suppressive role in acute EAE whereas TCR gamma delta+ T cells are not involved in the development of or recovery from the disease.

摘要

为阐明自然杀伤细胞(NK细胞)和T细胞受体γδ+ T细胞在Lewis大鼠诱导的急性实验性自身免疫性脑脊髓炎(EAE)中的作用,运用多种方法研究了这些细胞的分布、数量及功能。免疫组织化学和流式细胞术分析显示,在EAE高峰期,一定数量的NK细胞(占总炎性细胞的17%)浸润中枢神经系统(CNS),且主要位于血管周围区域。另一方面,在CNS中几乎未发现T细胞受体γδ+ T细胞。NK-T(NKR-P1+TCRαβ+)细胞数量很少,在CNS和淋巴器官中数量也未增加。在使用YAC-1细胞的细胞毒性试验中,从EAE高峰期大鼠脾脏分离的效应细胞与从正常对照大鼠分离的效应细胞表现出基本相同的细胞毒性,尽管NK细胞总数降至正常大鼠的五分之一。此外,体内给予抗NK细胞抗体(3.2.3和抗去唾液酸GM1)而非抗TCRγδ(V65)抗体,会加重EAE的临床症状,并在一些大鼠中诱发致命性EAE。这些发现表明,NK细胞在急性EAE中发挥抑制作用,而T细胞受体γδ+ T细胞不参与该疾病的发生发展或恢复过程。

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