Okuda Y, Sakoda S, Bernard C C, Fujimura H, Saeki Y, Kishimoto T, Yanagihara T
Department of Neurology, Osaka University Medical School, Suita, Japan.
Int Immunol. 1998 May;10(5):703-8. doi: 10.1093/intimm/10.5.703.
The role of IL-6 in experimental autoimmune encephalomyelitis (EAE) provoked by myelin oligodendrocyte glycoprotein (MOG) was investigated using IL-6-deficient mice. We show here that IL-6-deficient mice were resistant to the MOG-induced EAE as compared to wild-type mice (one out of 18 versus 17 out of 20). The delayed-type hypersensitivity response, lymphocyte proliferation response and antibody reactivity to MOG in IL-6-deficient mice were significantly lower than those in wild-type mice. Furthermore, the histological examination revealed that no infiltration of inflammatory cells was observed in the central nervous system of IL-6-deficient mice. These results indicate that IL-6 may play a crucial role in the induction phase of EAE. Given the potential relevance of this animal model for multiple sclerosis (MS), it is possible that anti-IL-6 therapy may be useful in the prevention of relapses of MS.
利用白细胞介素-6（IL-6）基因缺陷小鼠，研究了IL-6在髓鞘少突胶质细胞糖蛋白（MOG）诱发的实验性自身免疫性脑脊髓炎（EAE）中的作用。我们在此表明，与野生型小鼠相比，IL-6基因缺陷小鼠对MOG诱导的EAE具有抗性（18只中有1只发病，而20只野生型小鼠中有17只发病）。IL-6基因缺陷小鼠的迟发型超敏反应、淋巴细胞增殖反应以及对MOG的抗体反应性均显著低于野生型小鼠。此外，组织学检查显示，在IL-6基因缺陷小鼠的中枢神经系统中未观察到炎性细胞浸润。这些结果表明，IL-6可能在EAE的诱导阶段起关键作用。鉴于该动物模型与多发性硬化症（MS）的潜在相关性，抗IL-6疗法可能对预防MS复发有用。
