{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,25]],"date-time":"2025-10-25T13:57:14Z","timestamp":1761400634377},"reference-count":28,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2013,11,26]],"date-time":"2013-11-26T00:00:00Z","timestamp":1385424000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["2013CB966900"],"award-info":[{"award-number":["2013CB966900"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["RO1AI083294","R21 NS082902"],"award-info":[{"award-number":["RO1AI083294","R21 NS082902"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Immunol Cell Biol"],"published-print":{"date-parts":[[2014,2]]},"abstract":"<jats:p>Glatiramer acetate (GA) is one of the first\u2010line disease\u2010modifying medications that have been approved for the treatment of multiple sclerosis <jats:italic>via<\/jats:italic> 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\u2013Barr\u00e9 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)\u2010stimulated auto\u2010immune T\u2010cell proliferation <jats:italic>in vitro<\/jats:italic>. GA administrated at 10 days after induction of EAN when neurological sign became apparent also ameliorated the severity of disease, inhibited T\u2010cell 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.<\/jats:p>","DOI":"10.1038\/icb.2013.81","type":"journal-article","created":{"date-parts":[[2013,11,26]],"date-time":"2013-11-26T10:38:07Z","timestamp":1385462287000},"page":"164-169","source":"Crossref","is-referenced-by-count":12,"title":["Glatiramer acetate ameliorates experimental autoimmune neuritis"],"prefix":"10.1111","volume":"92","author":[{"given":"Cun\u2010Jin","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital Tianjin China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hui","family":"Zhai","sequence":"additional","affiliation":[{"name":"Department of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital Tianjin 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