The chemokine system in experimental autoimmune encephalomyelitis

Abstract

Chemokines chemoattract selected populations of inflammatory cells towards sites of inflammation in a gradient-dependent fashion, and also activate both recruited and resident inflammatory cells. Chemokines act on target cells through G-protein-coupled seven-transmembrane-domain receptors. High expression of several chemokines was found in the CNS during EAE. Cells expressing these chemokines were predominantly astrocytes and macrophages/microglia. In addition to chemokines, expression of several chemokine receptors was reported in EAE. Amelioration of EAE by anti-chemokine antibodies and studies in knock-out mice confirm the important roles of some chemokines in EAE pathogenesis. In the last several years many reports have been published addressing chemokine expression in multiple sclerosis. These results resemble results obtained earlier in EAE. Taken together, these data suggest that chemokine system may be a promising target for future treatment methods of multiple sclerosis.