Multiple sclerosis is a disease of the central nervous system, resulting in the\r\ndemyelination of neurons, causing mild to severe symptoms. Several anti-inflammatory\r\ntreatments now play a significant role in ameliorating the disease. Glatiramer acetate (GA)\r\nis a formulation of random polypeptide copolymers for the treatment of relapsing-remitting\r\nMS by limiting the frequency of attacks. While evidence suggests the influence of GA on\r\ninflammatory responses, the targeted molecular mechanisms remain poorly understood.\r\nHere, we review the multiple pharmacological modes-of-actions of glatiramer acetate in\r\ntreatment of multiple sclerosis. We discuss in particular a newly discovered interaction\r\nbetween the leukocyte-expressed integrin M2 (also called Mac-1, complement receptor 3,\r\nor CD11b/CD18) and perspectives on the GA co-polymers as an influence on the function\r\nof the innate immune system.
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