Lee S C, Moore G R, Golenwsky G, Raine C S
Department of Pathology (Neuropathology), Albert Einstein College of Medicine, Bronx, NY 10461.
J Neuropathol Exp Neurol. 1990 Mar;49(2):122-36. doi: 10.1097/00005072-199003000-00005.
Central nervous system (CNS) tissue was studied by immunocytochemistry and electron microscopy from three cases of multiple sclerosis (MS) in which evidence of ongoing myelin breakdown could be documented. The study focussed upon the role of glial cells in the pathogenesis of demyelination. In acute MS, demyelination involved the vesicular dissolution of myelin from intact axons and a paucity of fibrillary astrogliosis. Foamy macrophages, many of them probably derived from transformed and recently proliferated microglia, contained recognizable myelin debris and lipid droplets and were abundant throughout the lesions. These cells formed the major phagocytic population and stained positively for class II major histocompatibility complex antigens (HLA-DR; Ia). In acute MS lesions, rounded astrocytes were encountered which possessed membrane-bound compartments enclosing phagocytosed fragments of myelin basic protein-positive debris. Despite the superficial resemblance of these cells to foamy macrophages, the presence of intermediate filaments, glycogen granules and diffuse glial fibrillary acidic protein positivity supported an astroglial identity. Astrocyte processes were involved in myelin removal and invested recently demyelinated axons. Hypertrophic fibrous astrocytes were common in chronic active lesions, were capable of myelin degradation and on occasion, contained myelin debris attached to clathrin-coated pits. These astrocytes were sometimes Ia+. Oligodendrocytes were depleted from the center of active lesions but were numerous at the lesion margin, suggesting survival and proliferation. They stained positively for myelin-associated glycoprotein, a marker for immature oligodendrocytes. However, they were invariably Ia-. The findings confirm and further support a role for the astrocyte as both an antigen presenting cell and a phagocyte in the CNS during MS.
对3例多发性硬化症（MS）患者的中枢神经系统（CNS）组织进行了免疫细胞化学和电子显微镜研究，这些病例中有正在进行的髓鞘破坏的证据。该研究聚焦于神经胶质细胞在脱髓鞘发病机制中的作用。在急性MS中，脱髓鞘涉及完整轴突上髓鞘的泡状溶解以及纤维性星形胶质细胞增生不足。泡沫状巨噬细胞，其中许多可能源自转化和近期增殖的小胶质细胞，含有可识别的髓鞘碎片和脂滴，且在整个病变中大量存在。这些细胞构成了主要的吞噬细胞群体，并对II类主要组织相容性复合体抗原（HLA - DR；Ia）呈阳性染色。在急性MS病变中，可遇到圆形星形胶质细胞，其具有膜结合小室，内含吞噬的髓鞘碱性蛋白阳性碎片。尽管这些细胞表面上与泡沫状巨噬细胞相似，但中间丝、糖原颗粒的存在以及弥漫性胶质纤维酸性蛋白阳性支持其星形胶质细胞的身份。星形胶质细胞的突起参与髓鞘清除，并包绕最近脱髓鞘的轴突。肥大的纤维性星形胶质细胞在慢性活动性病变中常见，能够进行髓鞘降解，有时还含有附着于网格蛋白包被小窝的髓鞘碎片。这些星形胶质细胞有时Ia阳性。少突胶质细胞在活动性病变中心减少，但在病变边缘大量存在，提示其存活和增殖。它们对髓鞘相关糖蛋白呈阳性染色，这是未成熟少突胶质细胞的标志物。然而，它们始终Ia阴性。这些发现证实并进一步支持了星形胶质细胞在MS期间作为CNS中的抗原呈递细胞和吞噬细胞的作用。
