Multiple sclerosis is an autoimmune disease with classical traits of demyelination, axonal damage, and neurodegeneration. The migration of autoimmune T cells and macrophages from blood to central nervous system as well as the destruction of blood brain barrier are thought to be the major processes in the development of this disease. Chemokines, which are small peptide mediators, can attract pathogenic cells to the sites of inflammation. Each helper T cell subset expresses different chemokine receptors so as to exert their different functions in the pathogenesis of MS. Recently published results have shown that the levels of some chemokines and chemokine receptors are increased in blood and cerebrospinal fluid of MS patients. This review describes the advanced researches on the role of chemokines and chemokine receptors in the development of MS and discusses the potential therapy of this disease targeting the chemokine network. 1. Introduction Multiple sclerosis (MS), which was first described by Carswell, has been believed to be a chronic neuroinflammatory autoimmune disease with a still unknown etiology [1–3]. It is characterized by central nervous system (CNS) dysfunction, visual disorder, and motor deficits. MS is the most common cause of neurological disability in young adults [4]. Typically, the disease usually starts at the age of 20–40, being twice common in women as men [5]. Although the course of MS is variable, it is believed that there are different four patterns including relapsing-remitting multiple sclerosis (RRMS), primary progressive multiple sclerosis (PPMS), secondary progressive multiple sclerosis (SPMS), and primary-relapsing multiple sclerosis (PRMS) [6–8]. The pathogenesis of MS is still not well understood. As a multifactorial disease, MS is caused by some combination factors including viral infection, environmental factors, genetic predisposition, and autoimmune inflammation. Furthermore, recent data suggest that autoimmune inflammation plays a more important role in the development of this disease [9]. Although both the humoral and cellular immune responses are involved in the demyelinated tissue in MS, it is widely held that the cellular immune response is more crucial during MS development. Owing to the blood brain barrier (BBB) and blood cerebrospinal fluid barrier (BCB) involved, which provide an anatomic barrier to prevent free exchange of some substances between cerebrospinal fluid and blood to the CNS, the pathogenesis of CNS disease is different from other inflammatory diseases [5]. In some cases such as viral infection
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