These factors have previously been demonstrated to promote EAE pathogenesis and multiple sclerosis lesion formation; MMP-2 by facilitating immune cell migration out of the PVS and into the CNS parenchyma,8,9,41 CCL-2 through its chemotactic effects on infiltrating monocytes45,46 and GM-CSF via its effects on monocyte recruitment and pathogenic T-cell activity in the acute phase37,55,56 with pleiotropic effects on tissue damage in the chronic phase.57 The gene discussed is CCL2; the disease is multiple sclerosis.