ATG-dependent phagocytosis in dendritic cells drives myelin-specific CD4⁺ T cell pathogenicity during CNS inflammation.

ABSTRACT: Although reactivation and accumulation of autoreactive CD4⁺ T cells within the CNS are considered to play a key role in the pathogenesis of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), the mechanisms of how these cells recognize their target organ and induce sustained inflammation are incompletely understood. Here, we report that mice with conditional deletion of the essential autophagy protein ATG5 in classical dendritic cells (DCs), which are present at low frequencies in the nondiseased CNS, are completely resistant to EAE development following adoptive transfer of myelin-specific T cells and show substantially reduced in situ CD4⁺ T cell accumulation during the effector phase of the disease. Endogenous myelin pepti

SUBMITTER: Keller CW 

PROVIDER: S-EPMC5748192 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature