Weber Martin S, Hohlfeld Reinhard, Zamvil Scott S
Department of Neurology and Program in Immunology, University of California, San Francisco, CA 94143, USA.
Neurotherapeutics. 2007 Oct;4(4):647-53. doi: 10.1016/j.nurt.2007.08.002.
Glatiramer acetate (GA) (Copolymer-1, Copaxone, Teva, Israel, YEAK) is a polypeptide-based therapy approved for the treatment of relapsing-remitting multiple sclerosis. Most investigations have attributed the immunomodulatory effect of GAs to its capability to alter T-cell differentiation. Specifically, GA treatment is believed to promote development of Th2-polarized GA-reactive CD4(+) T-cells, which may dampen neighboring inflammation within the central nervous system. Recent reports indicate that the deficiency in CD4(+)CD25(+)FoxP3(+) regulatory T-cells in multiple sclerosis is restored by GA treatment. GA also exerts immunomodulatory activity on antigen presenting cells, which participate in innate immune responses. These new findings represent a plausible explanation for GA-mediated T-cell immune modulation and may provide useful insight for the development of new and more effective treatment options for multiple sclerosis.
醋酸格拉替雷(GA)(共聚-1、考帕松、梯瓦制药,以色列,耶路撒冷)是一种获批用于治疗复发缓解型多发性硬化症的基于多肽的疗法。大多数研究将GA的免疫调节作用归因于其改变T细胞分化的能力。具体而言,GA治疗被认为可促进向Th2极化的GA反应性CD4(+) T细胞的发育,这可能会减轻中枢神经系统内邻近部位的炎症。最近的报告表明,GA治疗可恢复多发性硬化症患者CD4(+)CD25(+)FoxP3(+)调节性T细胞的缺乏。GA还对抗抗原呈递细胞发挥免疫调节活性,抗原呈递细胞参与固有免疫反应。这些新发现为GA介导的T细胞免疫调节提供了一个合理的解释,并可能为开发新的、更有效的多发性硬化症治疗方案提供有用的见解。