Glatiramer

The mechanism of action of glatiramer acetate has not been fully elucidated; however, it is thought to act by modifying immune processes involved in the pathogenesis of multiple sclerosis (MS). MS is characterized by damage to the myelin layer that covers nerve cells (demyelination) and axonal degeneration. Also, it has been suggested that the myelin basic protein (MBP), a myelin autoantigen, plays a role in the development of MS.

Several mechanisms of action have been proposed. For instance, glatiramer acetate binds strongly to several major histocompatibility complex (MHC) class II molecules on MBP-specific antigen-presenting cells, preventing MBP from stimulating these cells. Glatiramer acetate also has the ability to shift the immune system from a pro-inflammatory to an anti-inflammatory pattern. It inhibits the secretion of pro-inflammatory cytokines (IL-2, IL-12, IFNγ, TNF) released by T helper 1 (Th1) cells, and induces T helper 2 (Th2) suppressor cells that are able to cross the blood-brain barrier and produce anti-inflammatory cytokines (IL-4, IL-5, IL-13, IL-10, TGF-β). It has also been suggested that glatiramer acetate induces the production of T-regulatory cells associated with the suppression of MS, such as CD4+, CD8+ and CD4+CD25+ cells.