Among these subsets are the B10 cells (CD24hiCD27+) which are known to suppress monocyte inflammatory functions including TNFα production [6], immature or transitional B cells (CD24hiCD38hi) which decrease IFNγ and TNF production [7], and the plasmablasts (CD38hiCD27+) which were reported to suppress the DC ability to generate pathogenic CD4+ T cells in a mouse model of experimental autoimmune encephalomyelitis [8]. This evidence concerns the gene TNF and experimental autoimmune encephalomyelitis.