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对醋酸格拉替雷作用机制的最新认识。

Recent insights into the mechanism of action of glatiramer acetate.

机构信息

Division of Neurology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, 350 West Thomas Road, Phoenix, AZ 85013, USA.

出版信息

J Neuroimmunol. 2011 Jun;235(1-2):9-17. doi: 10.1016/j.jneuroim.2011.01.009. Epub 2011 Mar 13.

Abstract

Glatiramer acetate (GA, Copaxone®, co-polymer 1) is an immunomodulatory therapy approved in 1996 by the United States Food and Drug Administration for treatment of relapsing-remitting multiple sclerosis. GA has a good safety profile, moderate efficacy, and a unique mode of action. Recent evidence in an animal model of MS, experimental autoimmune encephalomyelitis (EAE), suggests that GA effects on NK cells and B cells may contribute to therapeutic efficacy. We review the mechanism of action of GA, with particular focus on recent data suggesting a role for regulatory B cells.

摘要

醋酸格拉替雷(GA,Copaxone®,共聚物 1)是一种免疫调节疗法,于 1996 年获得美国食品和药物管理局批准,用于治疗复发缓解型多发性硬化症。GA 具有良好的安全性、中等的疗效和独特的作用模式。最近在多发性硬化症的动物模型——实验性自身免疫性脑脊髓炎(EAE)中的证据表明,GA 对自然杀伤细胞和 B 细胞的作用可能有助于其治疗效果。我们综述了 GA 的作用机制,特别关注最近的数据表明调节性 B 细胞可能发挥作用。

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