Experimental autoimmune encephalomyelitis (EAE) is an animal model of human autoimmune diseases in general, and multiple sclerosis (MS) in particular [2]. The animal disease is mediated through a network of cells; encephalitogenic CDThelper (CD4Th1) cells are activated in the peripheral lymph nodes following immunization for EAE, and migrate to the central nervous system where they induce activation of microglia, macrophages and dendritic cells (DCs). The resultant inflammation causes demyelination of neurons, prompting the presentation of myelin basic protein (MBP) to additional encephalitogenic T cell populations in the cervical lymph nodes by migratory DCs. The spontaneous recovery that occurs following autoimmune episodes is associated with the induction of apoptosis in encephalitogenic CD4Th1 cells by a CD8 regulatory T cell (CD8Treg) population [1,6]. Tang et al [7] demonstrated a mechanism where CD4Treg cells assist DCs in priming CD8Treg cells, which mediate down-regulation of the autoimmune response through selective apoptotic elimination of CD4Th1 cells.