Deletion of indoleamine 2,3 dioxygenase (Ido)1 but not Ido2 exacerbates disease symptoms of MOG_35-55-induced experimental autoimmune encephalomyelitis.

ABSTRACT: Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) with pathological features of inflammation, demyelination, and neurodegeneration. Several lines of evidence suggest that the enzymes indoleamine 2,3-dioxygenase (Ido)1 and/or Ido2 influences susceptibility to autoimmune diseases. Deletion of Ido1 exacerbates experimental autoimmune encephalomyelitis (EAE) an animal model of MS. However, no data exist on the role of Ido2 in the pathogenesis of EAE. We investigated whether deletion of Ido2 affected the pathogenesis of EAE. Temporal expression of interferon gamma (Ifng), Ido1 variants, Ido2 variants, as well as genes encoding enzymes of the kynurenine pathway in the spleen and spinal cord of C57BL/6 mice with or witho

SUBMITTER: Wetzel LA 

PROVIDER: S-EPMC8474387 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature