Archambault Angela S, Sim Julia, McCandless Erin E, Klein Robyn S, Russell John H
Department of Molecular Biology and Pharmacology, Washington University School of Medicine, 660 S. Euclid Ave., St. Louis, MO 63110, USA.
J Neuroimmunol. 2006 Dec;181(1-2):122-32. doi: 10.1016/j.jneuroim.2006.08.012. Epub 2006 Oct 9.
Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis and is characterized by an infiltrate of predominantly T cells and macrophages in the spinal cord and brain. In both the spinal cord and the cerebellum, Th1 cells direct inflammation to antigen-rich white matter tracts, and there is a TNFR1-dependent recruitment of CD11b(hi) cells in both regions. In the spinal cord, parenchymal invasion, demyelination and clinical symptoms are associated with TNFR1-dependant parenchymal induction (especially astrocytes) of VCAM-1 and CXCL2. None of these events occur in the cerebellum despite the fact that an inflammatory infiltrate accumulates in the perivascular space. Therefore regional specificity in astrocyte responses to inflammatory cytokines may regulate regional parenchymal infiltration and pathogenesis.
实验性自身免疫性脑脊髓炎（EAE）是多发性硬化症的动物模型，其特征是脊髓和大脑中主要有T细胞和巨噬细胞浸润。在脊髓和小脑中，Th1细胞将炎症导向富含抗原的白质束，并且在这两个区域都有TNFR1依赖性的CD11b(hi)细胞募集。在脊髓中，实质侵袭、脱髓鞘和临床症状与TNFR1依赖性的实质诱导（尤其是星形胶质细胞）VCAM-1和CXCL2有关。尽管炎症浸润在血管周围间隙中积累，但这些事件在小脑中均未发生。因此，星形胶质细胞对炎性细胞因子反应的区域特异性可能调节区域实质浸润和发病机制。
