IL2 and myeloid sarcoma: Various potential mechanisms have been proposed based on work done in the EAE model of MS: 1) circulating autoantibodies to myelin proteins may be targeted by IVIg; 2) IVIg can induce the expansion of regulatory T cells which can modulate the immune response in MS; 3) IVIg can downregulate pro-inflammatory cytokines such as IL-2, IFN-γ; 4) IVIg may prevent activated complement components from attaching to the surface of oligodendrocytes and myelin proteins [14], [21]–[24].