Abstract
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.
Highlights
Multiple sclerosis (MS) is a chronic inflammatory autoimmune disease in central nervous system (CNS) characterized by demyelination as well as axonal and neuronal degeneration
Th17 cells were found in the brain lesions of patients with MS; IL-17 expression was elevated in the serum and cerebrospinal fluid (CSF) of patients with MS [6]
It was first synthesized to mimic the encephalitogenic properties of myelin basic protein (MBP), one of the major myelin autoantigen involved in the induction of EAE, the animal model of MS
Summary
Multiple Sclerosis (MS) is a chronic inflammatory demyelinating disease of central nervous system (CNS), characterized by myelin destruction, loss of oligodendrocytes, axonal damage and astrogliosis [1]. It is the most common neurological disorder among young adults in which women are affected twice as frequently as men [2]. Current concepts assume that the pathogenesis of MS involve multiple factors including genetic predisposition, environmental factors, immune dysregulation, and viral infections. The breakdown of immune tolerance to self-antigens in genetically susceptible individuals is thought to be a key event in the development of MS [3,4]
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