Glatiramer acetate ameliorates experimental autoimmune neuritis. Issue 2 (26th November 2013)

• Record Type: Journal Article
• Authors: Zhang, Cun‐Jin; Zhai, Hui; Yan, Yaping; Hao, Junwei; Li, Min‐Shu; Jin, Wei‐Na; Su, Ning; Vollmer, Timothy L; Shi, Fu‐Dong
• Is Part Of: Immunology and cell biology. Volume 92:Issue 2(2014)
• Page Start: 164
• Page End: 169
• Publication Date: 2013-11-26
• Subjects: experimental autoimmune neuritis -- Glatiramer acetate -- Guillain–Barré syndrome -- multiple sclerosis; Immunology -- Periodicals; Cytology -- Periodicals; 616.079
• DOI: 10.1038/icb.2013.81
• Languages: English
• ISSNs: 0818-9641

Abstract

Abstract : Glatiramer acetate (GA) is one of the first‐line disease‐modifying medications that have been approved for the treatment of multiple sclerosis via immune modulatory mechanisms. However, it remains unclear whether the immunomodulation effect of GA is central nervous system (CNS) antigen specific. Here, we explored the mechanism of action of GA by subcutaneously injecting GA in experimental autoimmune neuritis (EAN) rats, an animal model for Guillain–Barré syndrome (GBS). Clinical, electrophysiological and histological findings showed that neurological deficits, demyelination and axonal injury of sciatic nerves were all significantly attenuated in Lewis rats when GA was administered before immunization with peripheral nervous system antigen P0. Our results further demonstrated that GA treatment inhibited either P0 or myelin basic protein (MBP) (CNS antigen)‐stimulated auto‐immune T‐cell proliferation in vitro . GA administrated at 10 days after induction of EAN when neurological sign became apparent also ameliorated the severity of disease, inhibited T‐cell response to P0 and MBP and induced shift of proinflammatory and immune modulatory cytokines. Collectively, our findings suggested that GA attenuated neurological deficits in EAN rats and that the immune modulatory mechanisms of GA were not CNS antigen specific.