Multiple sclerosis (MS) is an inflammatory disease of the central nervous system characterized by demyelination and axonal damage. Although the exact pathophysiology is unknown, apoptosis plays a crucial role. Here, we studied the role of the pro-apoptotic gene Bax in myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), the animal model for MS. We demonstrate that the clinical signs were markedly reduced in the EAE Bax-deficient mice as compared to wild type (2.3±0.5 vs. 1.02±0.32, respectively, P<0.05). Bax-deficient mice demonstrated less inflammatory infiltration and axonal damage, although they showed similar T-cell immune potency. In conclusion, ablation of the bax gene attenuates the severity of MOG-induced EAE and emphasizes the importance of apoptosis in the pathogenesis of EAE and MS.
- Bax-deficient mice
- Experimental autoimmune encephalomyelitis
- Multiple sclerosis
- Myelin oligodendrocyte glycoprotein