Zhang Guang-Xian, Yu Shuo, Gran Bruno, Li Jifen, Calida Divina, Ventura Elvira, Chen Xiaohan, Rostami Abdolmohamad
Department of Neurology, Thomas Jefferson University, 1025 and Walnut Street, Suite 310, Philadelphia, PA 19107-5083, USA.
J Neuroimmunol. 2004 Mar;148(1-2):1-10. doi: 10.1016/j.jneuroim.2003.10.057.
To characterize T cell and antibody responses in remitting-relapsing experimental autoimmune encephalomyelitis (RR-EAE), we compared myelin oligodendrocyte glycoprotein (MOG)-induced RR-EAE in C57BL/6 (B6) x SJL (F1) mice and chronic-progressive EAE (CP-EAE) in B6 mice at week 8 p.i. when clinical scores were comparable. Although these two strains exhibited similar inflammation/demyelination pattern and MOG-induced T cell responses, RR-EAE mice produced significantly higher levels of anti-MOG IgG1/IgG2a antibodies. Further, lymphocytes of RR-EAE mice proliferated vigorously to the secondary epitope myelin basic protein (MBP) 1-11. These results support a potential involvement of anti-MOG antibodies and epitope spreading in T cell responses in the development of MOG-induced RR-EAE model.
为了表征缓解复发型实验性自身免疫性脑脊髓炎(RR-EAE)中的T细胞和抗体反应,我们比较了C57BL/6(B6)×SJL(F1)小鼠中髓鞘少突胶质细胞糖蛋白(MOG)诱导的RR-EAE和B6小鼠中慢性进行性EAE(CP-EAE)在感染后第8周时的情况,此时临床评分相当。尽管这两种品系表现出相似的炎症/脱髓鞘模式以及MOG诱导的T细胞反应,但RR-EAE小鼠产生的抗MOG IgG1/IgG2a抗体水平显著更高。此外,RR-EAE小鼠的淋巴细胞对二级表位髓鞘碱性蛋白(MBP)1-11有强烈增殖反应。这些结果支持抗MOG抗体和表位扩展可能参与了MOG诱导的RR-EAE模型发展过程中的T细胞反应。