In contrast to other immunomodulatory MS therapies, GA has a distinct mechanism of action: GA demonstrates an initial strong promiscuous binding to major histocompatibility complex molecules and consequent competition with various (myelin) antigens for their presentation to T cells. In addition, antigen-based therapy generating a GA-specific immune response seems to be the prerequisite for GA therapy. GA treatment induces an in vivo change of the frequency, cytokine secretion pattern and the effector function of GA-specific CD4+ and CD8+ T cells, probably by affecting the properties of antigen-presenting cells such as monocytes and dendritic cells. As demonstrated extensively in animal experiments, GA-specific, mostly, T helper 2 cells migrate to the brain and lead to in situ bystander suppression of the inflammatory process in the brain. Furthermore, GA-specific cells in the brain express neurotrophic factors like the brain-derived neurotrophic factor (BDNF) in addition to anti-inflammatory T helper 2-like cytokines. This might help tip the balance in favor of more beneficial influences because there is a complex interplay between detrimental and beneficial factors and mediators in the inflammatory milieu of MS.
In Multiple Sclerosis (MS) and its animal model, Experimental Autoimmune Encephalomyelitis (EAE), the immune system reacts against myelin constitutes in the central nervous system (CNS), initiating a detrimental inflammatory cascade that leads to demyelination as well as axonal and neuronal pathology. The amino acid copolymer glatiramer acetate (GA) is an approved first-line treatment for MS that has a unique mode of action. Accumulated evidence from EAE-induced animals and from MS patients indicates that GA affects various levels of the innate and the adaptive immune response, generating deviation from the pro-inflammatory to the anti-inflammatory pathway. In view of its immunomodulatory activity, the beneficial effect of GA in various models of other autoimmune related pathologies, such as immune rejection and inflammatory bowel disease (IBD) is noteworthy.
Storage conditions: Store in a refrigerator in a well-closed container
Packaging: 1th polyethylene plastic bag. 2th. Three layered aluminum foil.