These pathways are also capable of suppressing bystander inflammation; for example infection of EAE mice with Schistosoma mansoni induced regulatory macrophages capable of modulating CNS inflammation (18), whereas immunizing with egg antigens from either S. mansoni or S. japonicum suppressed EAE progression by inducing Th2-deviation and IL-4 production, resulting in reduced MOG-specific Th1 and Th17 cytokines (19, 20). The gene discussed is IL4; the disease is infection.