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Multiple sclerosis (MS) is an inflammatory demyelinating disorder of the central nervous system (CNS).This autoimmune disease is more common in women than in men.In the study, the neuronal and immune injury in different gender C57BL/6 mice with experimental autoimmune encephalomyelitis (EAE), an animal model of MS, were observed.The female and male mice with EAE, was induced by immunization with peptide myelin oligodendrocyte glycoprotein (MOG) 35-55 and complete Freunds adjuvant (CFA) supplemented with pertussis toxin (PTX).The body weights and the neurological function scores of mice in different genders were assessed once a day for 40 days.The histopathologic changes in the brains of mice were observed by light microscope with hematoxylin-eosin (H&E) staining.The protein expression of myelin basic protein (MBP) and microtubule-associated protein (MAP)-2 in the brain of mice were measured by western-blot (WB) methods on day 22 post-immunization (PI) and by immunohistochemistry (IHC) on day 40 PI.The Interleukin (IL)-17A and forkhead box P3 (Foxp3) were assessed by IHC on day 22 and 40 PI.The results showed both female and male EAE mice developed with typical symptoms of neurological dysfunction and loss weights.A large number of inflammatory cells and nerve nucleus pyknotic were detected.The protein expression of MBP and MAP-2 was obviously decreased to different extents and the ratio of IL-17A/Foxp3 was dramatically enhanced in female and male EAE mice compared to normal mice, respectively.Further comparative studies between female and male mice revealed that the mortality and the neurological function scores were significantly increased, the latency was obviously shortered, MAP-2 were low expressed, while the ratio of IL-17A/Foxp3 was dramatically enhanced in male mice compared to the female mice.In conclusion, it suggested that the demyelination and axonal damage existed in mice with EAE, the imbalance between Th17 cells and Treg cells leaded to the occurrence of EAE.There were more levels of severity in male EAE mice.