Chunhua Chen
Multiple sclerosis (MS) is a chronic inflammatory autoimmune disease in central nervous system (CNS) characterized by demyelination as well as axonal and neuronal degeneration. Glatiramer acetate, is a mixture of synthetic polypeptides comprising four amino acids resembling the myelin basic protein (MBP), and approved as an immunoregulatory drug for the treatment of relapsing-remitting MS. The mechanism of action of GA in MS patients and the animal model experimental autoimmune encephalomyelitis (EAE) were extensively investigated over years. The cumulative findings indicate GA exerts its therapeutic activity by immunomodulating various levels of the immune response. This includes the blockade of major histocompatibility complex (MHC) molecules, T cell receptor antagonist, induction of GA-specific suppressor Th2 cells, an increase in frequency and function of CD4+CD25+FoxP3+ regulatory T cells, the down-regulation of Th1 and Th17 differentiation; the development of type II antigen presenting cells (APCs). In the review, we aim to provide a comprehensive overview of the immunoregulatory properties of GA in adaptive and innate immune response, in particular on the CD4+ effector T cells.
