Although the inflammatory CNS disease multiple sclerosis and its animal model EAE were historically associated with a Th1 immune response [17, 18], a pro-inflammatory role of IFN-γ was contradicted by substantially increased disease severity and mortality in mice deficient in IFN-γ (GKO) or the IFN-γR [19, 20]. This evidence concerns the gene IFNG and multiple sclerosis.