Department of Neuroinflammation, UCL Institute of Neurology, London, UK.
Mult Scler. 2012 Mar;18(3):286-98. doi: 10.1177/1352458511424309. Epub 2011 Sep 27.
Since CD8(+) T cells may be important in the pathogenesis of multiple sclerosis (MS), we examined their role in the DA rat experimental autoimmune encephalomyelitis (EAE) model induced by immunization with recombinant myelin oligodendrocyte glycoprotein (rMOG).
The inflammatory infiltrate in the spinal cord of affected animals was assessed by histology, electrophysiology and flow cytometry during the course of the disease (the first peak, remission and the second peak). The proportions of activated/memory effector (CD8(+)CD44(+)) and putative suppressor (CD8(+)CD28(-), CD8(+)CD25(high)) CD8(+) T cells in the draining lymph nodes were determined. To explore the role of CD8(+) T cells, similar experiments were performed in CD8(+) T cell depleted rats, before, during and after the first peak of the disease.
Throughout the disease, both CD4(+) T cells and macrophages/activated microglia outnumbered CD8(+) T cells within the spinal cord. The number of putative suppressor CD8(+) T cells increased significantly both during and after the first peak suggesting the induction of a regulatory CD8(+) T-cell response. However, antibody-mediated depletion of CD8(+) T cells before induction of the disease, or after the first peak, did not significantly alter the incidence, severity or course of rMOG-induced EAE.
The findings suggest that CD8(+) T cells do not play a significant role in the pathogenesis or regulation of EAE induced by rMOG in DA rats. In this respect, rMOG-induced EAE is not an appropriate model for studying the role of CD8(+) T cells in MS.
由于 CD8(+)T 细胞可能在多发性硬化症（MS）的发病机制中起重要作用，我们研究了它们在免疫重组髓鞘少突胶质细胞糖蛋白（rMOG）诱导的 DA 大鼠实验性自身免疫性脑脊髓炎（EAE）模型中的作用。
通过组织学、电生理学和流式细胞术在疾病过程中（第一高峰、缓解和第二高峰）评估受影响动物脊髓中的炎症浸润。确定引流淋巴结中激活/记忆效应（CD8(+)CD44(+））和假定的抑制（CD8(+)CD28(-），CD8(+)CD25(high））CD8(+)T 细胞的比例。为了探讨 CD8(+)T 细胞的作用，在疾病第一高峰之前、期间和之后，在 CD8(+)T 细胞耗竭大鼠中进行了类似的实验。
在整个疾病过程中，CD4(+)T 细胞和巨噬细胞/激活的小胶质细胞在脊髓内的数量均超过 CD8(+)T 细胞。在第一高峰期间和之后，假定的抑制性 CD8(+)T 细胞数量显著增加，提示诱导了调节性 CD8(+)T 细胞反应。然而，在疾病诱导之前或第一高峰后，通过抗体介导的 CD8(+)T 细胞耗竭，并不会显著改变 rMOG 诱导的 EAE 的发生率、严重程度或病程。
这些发现表明，CD8(+)T 细胞在 rMOG 诱导的 DA 大鼠 EAE 的发病机制或调节中不起重要作用。在这方面，rMOG 诱导的 EAE 不是研究 CD8(+)T 细胞在 MS 中作用的合适模型。
