CD4 and myeloid sarcoma: These effects on the generation of CD4+ T cell effector subsets known to cause disease may provide one possible explanation of the failure of the MSCs to modulate MOG35–55 EAE pathogenesis in this setting and have relevance to MS in which it has been postulated that heterogeneity of the disease may be partly determined by relative propensity for TH1 vs TH17 immune deviation [43].