TNFR2 signaling in oligodendrocyte precursor cells suppresses their immune-inflammatory function and detrimental microglia activation in CNS demyelinating disease.

ABSTRACT: Multiple Sclerosis (MS) is a chronic degenerative disease of the central nervous system (CNS) characterized by inflammation, demyelination, and progressive neurodegeneration. These processes, combined with the failure of reparative remyelination initiated by oligodendrocyte precursor cells (OPCs), lead to irreversible neurological impairment. The cytokine tumor necrosis factor (TNF) has been implicated in CNS repair via activation of its cognate receptor TNFR2 in glia. Here, we demonstrate the important role of TNFR2 in regulating OPC function in vivo during demyelinating disease, and that TNFR2 expressed in OPCs modulates OPC-microglia interactions. In Pdgfrα^CreERT:Tnfrsf1b^fl/fl:Eyfp mice with selective TNFR2 ablation in OPCs, we observed an earlier onset and disease

SUBMITTER: Desu HL 

PROVIDER: S-EPMC11624083 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature