Colocalization of lymphocytes bearing gamma delta T-cell receptor and heat shock protein hsp65+ oligodendrocytes in multiple sclerosis.
Colocalization of lymphocytes bearing gamma delta T-cell receptor and heat shock protein hsp65+ oligodendrocytes in multiple sclerosis.
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DOI：
10.1073/pnas.88.15.6452
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发表时间：
1991-08
影响因子：
11.1
通讯作者：
Krzysztof Selmaj;C. Brosnan;C. S. Raine
中科院分区：
文献类型：
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作者：
Krzysztof Selmaj;C. Brosnan;C. S. Raine
在13例多发性硬化症（MS）患者、4例炎症性非MS CNS疾病患者、6例其他神经系统疾病患者和3例非神经系统疾病患者的中枢神经系统（CNS）组织中，研究了携带γ δ T细胞受体（TCR γ δ）的T淋巴细胞的免疫细胞化学存在。43个MS病变中有28个含有TCR γ δ细胞，这些细胞最常见于慢性脱髓鞘区，与先前研究的CD4+， CD8+ (TCR α β)人群相反，后者主要见于更活跃的病变。一些TCR γ δ淋巴细胞形态异常，具有长树突，有时相互连接形成网络。由于人们普遍认为TCR γ δ淋巴细胞以细胞毒性方式与热休克蛋白（hsp）相关，因此我们研究了TCR γ δ细胞与65和70 kda的hsp （hsp65和hsp70）在MS病变中的共定位。Hsp65在含TCR γ δ淋巴细胞的慢性病变边缘的未成熟少突胶质细胞上表达。这些分子的共表达可能暗示了功能关系，可能对MS疾病过程的慢性性和中枢神经系统髓鞘再生的失败具有重要意义。
The presence of T lymphocytes bearing the gamma delta T-cell receptor (TCR gamma delta) has been studied immunocyto-chemically in central nervous system (CNS) tissue from 13 patients with multiple sclerosis (MS), 4 with inflammatory non-MS CNS disorders, 6 with other neurological diseases, and 3 with nonneurologic conditions. Twenty-eight of 43 MS lesions contained TCR gamma delta cells and these were most frequently found in chronically demyelinated areas, in contrast to the previously studied CD4+, CD8+ (TCR alpha beta) population, which predominated in more active lesions. Some TCR gamma delta lymphocytes had an unusual morphology with long dendritic processes, which were sometimes interconnected forming a network. Because it is generally believed that TCR gamma delta lymphocytes function in a cytotoxic fashion in association with heat shock proteins (hsp), we examined the colocalization of TCR gamma delta cells with 65- and 70-kDa hsp (hsp65 and hsp70) in MS lesions. Hsp65 was expressed on immature oligodendrocytes at the margins of chronic lesions containing TCR gamma delta lymphocytes. The coexpression of these molecules might imply functional relationships perhaps of significance to the chronicity of the MS disease process and the failure of CNS remyelination.