IMMUNOGENESIS OF MULTIPLE SCLEROSIS PLAQUE
IMMUNOGENESIS OF MULTIPLE SCLEROSIS PLAQUE
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DOI：
10.1016/0006-8993(71)90052-7
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发表时间：
1971-01-01
期刊：
影响因子：
2.9
通讯作者：
LUMSDEN, CE
中科院分区：
文献类型：
--
作者：
LUMSDEN, CE
多发性硬化症(MS)斑块的病理有其独特性，这一点经常被断言。这种“独一无二”的性质仅仅部分在于脱髓鞘的选择性(即保留轴突)，与少突胶质细胞溶解11和紧跟在脱髓鞘之后的星形细胞反应有关，如我们所示，这种脱髓鞘几乎立即“开启”胶质纤维生成(好像通过某种抑制机制)。但更多的人被忽视的一点是，MS病变的独特性还在于斑块的形式(已被不同地与之比较的“油滴”或“墨迹”)，在于它的强制性静脉关系15，最重要的是它的离心性扩散特性。多发性硬化症斑块确实在其边缘扩散或生长是一个非常重要的细节--其事实有效性必须仔细确定--因为如果这一结论被接受为真，那么所有与缺氧或转瞬即逝的血栓P1类似的致病假说都是站不住脚的。除了几乎不可能的、对斑块实际生长的视觉演示之外，需要对斑块进行极其仔细的病理分析，以说服自己相信这一结论的真实性。准确地说，这种分析最近再次进行了15，而早些时候已经陈述的判决11证实了这一点。斑块最初是围绕着小静脉的脱髓鞘环，然后逐渐和间歇性地扩大。这一解剖-病理事实(正如作者现在认为的那样)对于正确理解本文所追踪的MS斑块是至关重要的--因为无论受影响的CNS组织中的固有抗髓鞘因子的作用如何，导致MS斑块脱髓鞘扩大的大部分因素或机构来自中央静脉或小静脉(或其附近)，并从那里径向向外携带或扩散。刚才引用的主要研究中尝试的病理分析是本文将要阐述的案例的关键部分。
That there is a uniqueness in the pathology of the multiple sclerosis (MS) plaque has been frequently asserted. This' unique'quality lies only partly in the selective (ie axon-sparing) nature of the demyelination, associated with oligodendrogliolysis 11 and with an astrocytic reaction which follows closely upon the heels of this demyelination which, as we have shown 1,'switches on'gliofibrillogenesis almost immediately (as though by some mechanism of de-repression). But the point has been more frequently missed that the uniqueness of the MS lesion lies also in the form of the plaque ('oil-drop'or'ink-blot', as it has been variously compared with), in its obligatory venular relationship 15 and, above all, in its centrifugally-spreading character. That an MS plaque does spread or grow at its edges is a detail of enormous importance--the factual validity of which has to be carefully established--because this conclusion, if accepted as true, renders non-tenable all pathogenetic hypotheses along the lines of anoxia or evanescent thrombP 1. Short of the virtually impossible, a visual demonstration of the actual growth of a plaque, extremely careful pathological analysis of plaques is needed to convince oneself of the truth of this conclusion. Precisely this sort of analysis was again undertaken recently 15 and the verdict, already stated earlier 11, substantiated viz. that plaques begin as collars of demyelination round small veins and that they enlarge thereafter, both steadily and episodically. This anatomo-pathological fact (as the writer now takes it to be) is crucial to a proper understanding of the MS plaque as traced out in the present paper--for the reason that whatever the role of autochthonous antimyelin factors within the affected CNS tissues, the bulk of the factor or agency responsible for the demyelinative enlargement of the MS plaque is derived from the central vein or venule (or from the immediate vicinity thereof) and thence is carried or diffused radially outwards. The pathological analysis attempted in the major study just cited 15 is a critical part of the case to be made out in the present paper.