Multiple sclerosis. Interactions between oligodendrocytes and hypertrophic astrocytes and their occurrence in other, nondemyelinating conditions.
Multiple sclerosis. Interactions between oligodendrocytes and hypertrophic astrocytes and their occurrence in other, nondemyelinating conditions.
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发表时间：
1992-07
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通讯作者：
E. Wu;Raine Cs
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作者：
E. Wu;Raine Cs
背景以前已经描述了在解决多发性硬化（MS）病变中少突胶质细胞的增殖及其与肥大星形胶质细胞的相关性。实验设计不同年龄的中枢神经系统病变进行了检查，从9例MS的临床病史范围从8周到13年，在各种非MS条件。结果：在MS中，发现这些相关性最常发生在急性、活动性脱髓鞘（而不是消退）病变中。它们也发生在慢性活动性和慢性静止性MS斑块中以及病变附近显示髓鞘再生或正常髓鞘形成的区域中，尽管很少见。免疫细胞化学显示，少突胶质细胞的数量增加，并显示增强的HNK-1的反应，类似于以前的研究，声称这些细胞是最近的起源。超微结构上，病变中心的肥大星形胶质细胞通常没有形成的中间纤维束，而是显示出细颗粒状的细胞质。向周边，它们包含成束的细丝，并显示抗神经胶质细胞酸性蛋白抗体染色增加。的相互作用涉及密切的贴壁，少突胶质细胞和内化的星形胶质细胞，膜之间发生的专业化，提示的粘附事件。在各种非MS条件下也观察到相同的神经胶质相关性。在大多数后一种情况下，有中枢神经系统炎症和/或破坏的证据。结论：这些观察结果强调了在活动性MS病变中胶质细胞现象的频率增加，其在不同病因的疾病中的普遍存在，以及在评估归因于MS的现象的特异性时需要仔细检查控制中枢神经系统组织。这表明这些胶质细胞协会可能代表一种短暂的保护机制，并可能与局部细胞因子的产生有关。
BACKGROUND The proliferation of oligodendrocytes and their association with hypertrophic astrocytes has been previously described in resolving multiple sclerosis (MS) lesions. EXPERIMENTAL DESIGN Central nervous system lesions of different ages were examined from 9 cases of MS with clinical histories ranging from 8 weeks to 13 years and in a variety of non-MS conditions. RESULTS In MS, these associations were found to occur most frequently in acute, actively demyelinating (as opposed to resolving) lesions. They also occurred, albeit rarely, in chronic active and chronic silent MS plaques and in areas showing remyelination or normal myelination adjacent to lesions. Immunocytochemistry revealed that the oligodendrocytes occurred in increased numbers and displayed enhanced reactivity for HNK-1, similar to previous studies that claimed such cells to be of recent origin. Ultrastructurally, hypertrophic astrocytes in the lesion center usually possessed no formed bundles of intermediate filaments, but rather displayed a finely granular cytoplasm. Towards the perimeter, they contained bundles of filaments and showed increased staining with anti-glial fibrillary acidic protein antibody. The interactions involved the close apposition to, and internalization of oligodendrocytes by astrocytes, between which membrane specializations occurred, suggestive of an adhesion event. Identical glial associations were also seen in various non-MS conditions. In most of the latter cases, there was evidence of central nervous system inflammation and/or destruction. CONCLUSIONS These observations underscore the increased frequency of the glial cell phenomenon in active MS lesions, its ubiquity in diseases of different etiologies and the need for careful scrutiny of control central nervous system tissue in assessing the specificity of phenomena attributed to MS. It is suggested that these glial associations may represent a transient protective mechanism and may be related to local cytokine production.