To understand why remyelination fails in diseases such as multiple sclerosis (MS), I studied the cells and molecules involved in remyelination. I examined the cellular response to cuprizone-induced demyelination in C57B1/6 female mice. In response to the toxin cuprizone, microglia, macrophages, T cells and oligodendrocyte precursor cells (OPCs), accumulated in the corpus callosum. I have identified a novel population of CD11c-expressing microglia with potent antigen presenting capacity, which localized to the demyelinated corpus callosum following cuprizone treatment. A broad panel of chemokines were upregulated as early as 1 week following cuprizone treatment. Administration of one of them, an oligodendrocyte precursor cell growth factor, CXCL1, via adenoviral gene delivery to the CNS, did not affect OPC dynamics in the demyelinated corpus callosum. Insight into cells and molecules produced during demyelination/remyelination will be of use in designing new therapies for MS.