HMOX1 and experimental autoimmune encephalomyelitis: Chora and co-workers (66) reported that HO-1 expression dictated the pathologic outcome of experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis, and pharmacological induction of HO-1 suppressed the pathologic outcome of autoimmune neuro-inflammation associated with the development of EAE, presumably by inhibiting the expression of MHC class II on APCs and the reactivation of pathogenic CD4+ T cells within the central nerve system.