Expression of MCP-1 by reactive astrocytes in demyelinating multiple sclerosis lesions
Expression of MCP-1 by reactive astrocytes in demyelinating multiple sclerosis lesions
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DOI：
10.1016/s0002-9440(10)65249-2
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发表时间：
1999-01-01
影响因子：
6
通讯作者：
De Groot, CJA
中科院分区：
文献类型：
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作者：
Van der Voorn, P;Tekstra, J;De Groot, CJA
多发性硬化症（MS）的病理特征是血脑屏障（BBB）的破坏，伴随着巨噬细胞和T淋巴细胞浸润到中枢神经系统（CNS），这些细胞向CNS实质的迁移可能部分受到趋化因子的调节。因此，本研究的目的是通过对 MS 和正常对照病例死后脑组织的免疫组织化学研究强单核细胞和 T 细胞趋化因子单核细胞趋化蛋白 (MCP)-1 的细胞定位。根据特征性（免疫）组织化学染色模式对六名多发性硬化症患者和四名无脑部疾病史的患者的脑组织样本进行神经病理学分类。活动性脱髓鞘性多发性硬化症病变、慢性活动性脱髓鞘性多发性硬化症病变和正常对照大脑的冰冻组织切片仅用针对MCP-1的单克隆抗体进行免疫组织化学染色。在活动性脱髓鞘性 MS 病变中，如慢性活动性 MS 病变中，反应性肥大星形胶质细胞对 MCP-1 具有强烈的免疫反应性，而血管周围和实质泡沫状巨噬细胞不表达 MCP-1 蛋白。这些结果表明，β-趋化因子 MCP-1（由反应性肥大星形胶质细胞在体内合成）在髓磷脂降解巨噬细胞的募集和激活中发挥着重要作用，从而促进 MS 病变的演变。
The pathology of multiple sclerosis (MS) is characterized by breakdown of the blood-brain barrier (BBB), accompanied by infiltration of macrophages and T lymphocytes into the central nervous system (CNS), The migration of these cells into the CNS parenchyma may be partly regulated by chemokines. The aim of this study was therefore to investigate the cellular localization of the potent monocyte- and T-cell-attracting chemokine monocyte chemoattractant protein (MCP)-1 by immunohistochemistry on postmortem brain tissue from MS and normal control cases. Brain tissue samples of six MS patients and four patients without a history of brain disease were neuropathologically classified according to characteristic (immuno)histochemical staining patterns. Frozen tissue sections of active demyelinating MS lesions, chronic active demyelinating MS lesions, and normal control brain mere immunohistochemically stained with a monoclonal antibody directed against MCP-1. In active demyelinating MS lesions as web as in chronic active MS lesions, reactive hypertrophic astrocytes were strongly immunoreactive for MCP-1, whereas perivascular and parenchymal foamy macrophages did not express MCP-1 protein. These results suggest a significant role for the beta-chemokine MCP-1, synthesized in vivo by reactive hypertrophic astrocytes, in the recruitment and activation of myelin-degrading macrophages and thereby contributing to the evolution of MS lesions.