CCL2 and experimental autoimmune encephalomyelitis: The high levels of CCL2 that we found to be elicited in DRG neurons and satellite glial cells, as well as in Schwann cells in response to B. burgdorferi, could trigger mechanisms of demyelination in the PNS similar to those thought to cause CNS demyelination in MS and experimental autoimmune encephalomyelitis (EAE) [81,82].