Abstract
Glatiramer acetate (GA) is together with recombinant interferons beta the first disease modifying drugs in the treatment of patients with multiple sclerosis (MS). GA is underfined mixture of synthetic peptides which structures resemble myelin basic protein MBP, the principal target of auto reactive the cells in patients with MS.
GA is after subcutaneous administration internalised by dendritic cells in which is further processed and presented in complex with HLA II molecules in lymph nodes to T cells. T cells recognizing GA fragments are stimulated to the differentation to immunoregulatory subsets of Treg and Th2.
The harm immunopathological reactivity which hallmark is upregulated activity of Th17 and Th1 T cell is dampen by GA specific Treg and Th2 T cells. These cells are migrating to the brain displaying additional immunoregulatory effects.
In addition, various neurotrophic cytokines such as BDGF and NT-3,4 are produced by these cells resulting in reparation of demyelinated lesions thus preventing neurodegeneration. New glatiramoids are now introduced to the clinical practice.
Unique group of drugs called non-biological complex drugs in comprising glatiramoids. Results of experimental studies suggest that these new glatiramoids are different in their chemical nature and immunobiological activities compared to glatiramer acetate which seems currently irreplaceable in this regard.