Monocytes and macrophages play a pathogenic role in a number of autoimmune inflammatory diseases. Recent studies in experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis, have identified a critical chemokine-mediated mechanism of monocyte homing to the central nervous system (CNS). Here, we summarize the current findings in EAE, develop a rationale for targeting the chemokine axis in order to treat CNS inflammatory disease, and review currently available molecule-specific therapeutics that inhibit monocyte trafficking to the CNS.
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