Upregulation and coexpression of adhesion molecules correlate with relapsing autoimmune demyelination in the central nervous system.
Upregulation and coexpression of adhesion molecules correlate with relapsing autoimmune demyelination in the central nervous system.
复制标题
粘附分子的上调和共表达与中枢神经系统中的自身免疫性脱髓鞘相关。
DOI：
10.1084/jem.172.5.1521
复制
发表时间：
1990-11-01
影响因子：
15.3
通讯作者：
Raine, C S
中科院分区：
文献类型：
--
作者：
Cannella, B;Cross, A H;Raine, C S
研究了SJL小鼠慢性复发性实验性自身免疫性脑脊髓炎期间中枢神经系统（CNS）血管粘附分子的表达。研究了与细胞粘附相关的两种分子：小鼠淋巴结高内皮小静脉标志物MECA-325；细胞间粘附分子1的小鼠同源物MALA-2。在初始疾病期间，这两种分子的共表达上调发生在中枢神经系统。这与炎症细胞侵袭有关。在缓解期间，表达下调，随后每次复发都伴有相应的上调。因此，靶器官中粘附分子的上调和下调似乎是这种自身免疫性疾病中炎症过程的一个组成部分，并支持受体介导的炎症细胞侵袭与多发性硬化症发病机制相关的作用。
The expression of adhesion molecules on central nervous system (CNS) vessels was examined during chronic relapsing experimental autoimmune encephalomyelitis in the SJL mouse. Two molecules associated with cell adhesion were studied: MECA-325, a murine lymph node high endothelial venule marker; and MALA-2, the murine homologue of intercellular adhesion molecule 1. During initial disease, upregulated coexpression of these two molecules occurred in the CNS. This correlated with inflammatory cell invasion. During remission, expression was downregulated, and each subsequent relapse was accompanied by corresponding upregulation. Thus, up- and downregulation of adhesion molecules in the target organ appeared to form an integral part of the inflammatory process in this autoimmune condition and support a role for receptor-mediated inflammatory cell invasion of relevance to the pathogenesis of multiple sclerosis.