INFLAMMATION AND THE BRAIN

INFLAMMATION AND THE BRAIN
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DOI:
10.1007/bf03160168
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发表时间:
1993-05-01
期刊:
MOLECULAR AND CHEMICAL NEUROPATHOLOGY
影响因子:
--
通讯作者:
COMPSTON, A
COMPSTON, A
中科院分区:
其他
文献类型:
--
作者:
COMPSTON, A

文献摘要

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大脑中的炎症选择性地损害髓鞘,导致各种临床症状,其中最常见的是多发性硬化症。在这些疾病中,炎症和脱髓鞘的区域可以通过磁共振成像在生活中识别出来。发生在血脑屏障上的事件取决于T细胞的激活,T细胞的激活增加了中枢神经系统内的免疫监视。针对脑抗原激活的T细胞持续建立炎症脱髓鞘所需的条件,这依赖于局部细胞因子的释放,最终导致巨噬细胞或小胶质细胞清除少突胶质细胞及其髓鞘片层。这些相互作用包括存在于小胶质细胞上的抗体和补体Fc部分的受体与靶细胞上相应的配体结合。总之,来自临床和实验研究的证据为多发性硬化症患者的免疫治疗问题提供了理论基础。
Inflammation in the brain selectively damages the myelin sheath resulting in a variety of clinical syndromes of which the most common is multiple sclerosis. In these disorders, the areas of inflammation and demyelination can be identified in life by magnetic resonance imaging. Events occurring at the blood-brain barrier depend on T-cell activation, which increases immune surveillance within the central nervous system. T-cells activated against brain antigens persist to establish the conditions needed for inflammatory demyelination and this depends on local release of cytokines, culminating in removal of oligodendrocytes and their myelin lamellae by macrophages or microglia. These interactions involve binding between receptors present on microglia for the Fc portion of antibody and complement components to corresponding ligands on target cells. Taken together, the evidence from clinical and experimental studies provides a rationale for the issue of immunological treatments in patients with multiple sclerosis.