Galectin-3/MAC-2 in experimental allergic encephalomyelitis
Galectin-3/MAC-2 in experimental allergic encephalomyelitis
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DOI：
10.1006/exnr.1999.7229
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发表时间：
1999-12-01
影响因子：
5.3
通讯作者：
Rotshenker, S
中科院分区：
文献类型：
--
作者：
Reichert, F;Rotshenker, S
通过吞噬作用清除变性的髓鞘是创伤和疾病神经系统的发病机制和修复的中心。半乳糖凝集素-3/MAC-2是鼠和人单核细胞/巨噬细胞/小胶质细胞的分化和活化标志物。半乳糖凝集素-3/ MAC-2，沿着介导髓鞘吞噬作用的MAC-1，标志着巨噬细胞中的体内活化状态，其参与损伤的小鼠外周神经中的髓鞘变性和吞噬作用。相反，在损伤的CNS中体内表达高水平的MAC-1但极低水平的半乳糖凝集素-3/MAC-2，其中髓鞘变性和吞噬作用进展极慢。本研究旨在测试由半乳糖凝集素-3/MAC-2标记的活化状态是否存在于EAE小鼠的CNS中，伴随着自身免疫诱导的髓鞘变性和吞噬作用。用小鼠脊髓匀浆造成EAE。通过光学显微镜评估脱髓鞘，通过免疫细胞化学评估半乳糖凝集素-3/MAC-2、MAC-1和F4/80表达。我们目前的文件，半乳糖凝集素-3/MAC-2的表达上调，沿着MAC-1和F4/80，在脊髓和视神经的EAE小鼠的脱髓鞘和髓鞘变性的领域，在髓鞘吞噬小胶质细胞和巨噬细胞。共聚物1（醋酸格拉替雷）抑制EAE、脱髓鞘和半乳糖凝集素-3/MAC-2表达。因此，EAE发病机制涉及小胶质细胞和巨噬细胞中的活化状态，其特征在于半乳糖凝集素-3/MAC-2沿着MAC-1的表达。此外，在CNS中对损伤和自身免疫性攻击的体内应答在小胶质细胞和巨噬细胞的活化模式方面不同，这与半乳糖凝集素-3/MAC-2表达以及相应的髓鞘变性和吞噬作用的发生有关。(C)北京：科学出版社.
The removal of degenerating myelin by phagocytosis is central to pathogenesis and repair in traumatized and diseased nervous system. Galectin-3/MAC-2 is a differentiation and activation marker of murine and human monocytes/macrophages/microglia. Galectin-3/ MAC-2, along with MAC-1 that mediates myelin phagocytosis, marks an in vivo activation state in macrophages, which are involved in myelin degeneration and phagocytosis in injured mouse peripheral nerves. In contrast, high levels of MAC-1 but extremely low levels of Galectin-3/MAC-2 are expressed in vivo in injured CNS where myelin degeneration and phagocytosis progress extremely slowly The present study was aimed at testing whether an activation state marked by Galectin-3/MAC-2 is present in vivo in the CNS of EAE mice concomitant with autoimmune induced myelin degeneration and phagocytosis. EAE was inflicted by mouse spinal cord homogenate. Demyelination was assessed by light microscopy and Galectin-3/MAC-2, MAC-1, and F4/80 expression by immunocytochemistry. We presently document that Galectin-3/MAC-2 expression is up regulated, along with MAC-1 and F4/80, in spinal cords and optic nerves of EAE mice in areas of demyelination and myelin degeneration, in myelin phagocytosing microglia and macrophages. Copolymer 1 (Glatiramer acetate) suppresses EAE, demyelination, and Galectin-3/MAC-2 expression. EAE pathogenesis thus involves a state of activation in microglia and macrophages characterized by the expression Galectin-3/MAC-2 along with MAC-1. Furthermore, the in vivo responses to injury and autoimmune challenge in the CNS differ in the activation pattern of microglia and macrophages with regard to Galectin-3/MAC-2 expression and the corresponding occurrence of myelin degeneration and phagocytosis. (C) 1999 Academic Press.