Axonal damage has recently been recognized to be a key predictor of outcome in a number of diverse human CNS diseases, including multiple sclerosis (MS). The mechanism of axonal loss in MS is uncertain, but may involve axonal degeneration, which may be secondary to demyelination or immune cells attack directed to axonal components. We are interested in studying the molecular mechanism involving the crosstalk between the immune system and the CNS during axonal degeneration in an experimental autoimmune encephalomyelitis (EAE), a widely used animal model of MS.