Storch M K, Stefferl A, Brehm U, Weissert R, Wallström E, Kerschensteiner M, Olsson T, Linington C, Lassmann H
Neurological Institute, University of Vienna, Austria.
Brain Pathol. 1998 Oct;8(4):681-94. doi: 10.1111/j.1750-3639.1998.tb00194.x.
Multiple sclerosis is a chronic inflammatory disease characterized by perivenous inflammation and focal destruction of myelin. Many attempts have been undertaken previously to create animal models of chronic inflammatory demyelinating diseases through autoimmunity or virus infection. Recently, however, a new model of myelin oligodendrocyte glycoprotein (MOG) induced autoimmune encephalomyelitis became available, which, in a very standardized and predictable way, leads to chronic (relapsing or progressive) disease and widespread CNS demyelination. In the present study we actively induced MOG-experimental autoimmune encephalomyelitis (EAE) in different inbred rat strains using different immunization protocols. The pathology found in our models closely reflects the spectrum of multiple sclerosis (MS) pathology: Classical MS as well as variants such as optic neuritis, Devic's disease and Marburg's type of acute MS are mimicked in rats immunized with MOG antigen. Furthermore we demonstrate, that by using the proper strain/sensitization regime, subforms of MS such as for instance neuromyelitis optica can be reproducibly induced. Our study further supports the notion, that incidence and expression of the disease in this model, alike the situation in multiple sclerosis, is determined by genetic and environmental factors.
多发性硬化症是一种慢性炎症性疾病，其特征为静脉周围炎症和髓鞘的局灶性破坏。此前人们曾多次尝试通过自身免疫或病毒感染来建立慢性炎症性脱髓鞘疾病的动物模型。然而，最近出现了一种新的髓鞘少突胶质细胞糖蛋白（MOG）诱导的自身免疫性脑脊髓炎模型，该模型以非常标准化且可预测的方式导致慢性（复发或进展性）疾病以及广泛的中枢神经系统脱髓鞘。在本研究中，我们使用不同的免疫方案在不同的近交系大鼠品系中主动诱导MOG - 实验性自身免疫性脑脊髓炎（EAE）。我们模型中发现的病理学情况密切反映了多发性硬化症（MS）病理学的范围：在用MOG抗原免疫的大鼠中模拟了经典MS以及诸如视神经炎、视神经脊髓炎和马尔堡型急性MS等变体。此外，我们证明，通过使用合适的品系/致敏方案，可以可重复地诱导MS的亚型，例如视神经脊髓炎。我们的研究进一步支持了这样一种观点，即该模型中疾病的发病率和表现，与多发性硬化症的情况一样，由遗传和环境因素决定。
