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CELL-SPECIFIC REGULATION OF MIF DURING DEMYELINATION AND REMYELINATION
Åsa Fex Svenningsenand 3 co-authors
University of Southern Denmark
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS03-08AM-006
Presentation
Date TBA
Board: PS03-08AM-006
Event Information
Poster Board
PS03-08AM-006
Poster
View posterAbstract
Macrophage migration inhibitory factor (MIF) is often described as a pro-inflammatory cytokine that worsens neuroinflammatory disease. However, clinical data show that MIF levels are reduced in cerebrospinal fluid from patients with clinically isolated syndrome and relapsing remitting multiple sclerosis (RRMS), suggesting that MIF regulation in the central nervous system is stage- and cell-dependent. We investigated how MIF is regulated during demyelination and remyelination using the cuprizone model combined with primary neuronal and glial cultures.
After 6 weeks of cuprizone treatment, total brain MIF levels were significantly reduced, consistent with previous observations in RRMS. Immunohistochemical analyses showed that under normal conditions MIF is prominently expressed in cortical and hippocampal neurons in vivo. Following cuprizone-induced demyelination, neuronal MIF was reduced, coinciding with the decreased brain MIF levels. In contrast, MIF-positive oligodendrocyte precursor cells (OPCs) accumulated in the corpus callosum peaking during early remyelination, identifying OPCs as a major local source of MIF during repair.
In vitro, pharmacological inhibition of MIF impaired neurite outgrowth in primary cortical neurons. In glial cultures, MIF inhibition reduced microglial and astrocytic proliferation and dampened basal microglial activation, while increasing astrocytic GFAP expression. In OPCs, MIF promoted proliferation and migration under non-inflammatory conditions. Many of these effects were abolished by IFN-γ, highlighting inflammatory context as a key modifier of MIF regulation.
Together, these findings show that MIF is differentially regulated across CNS cell types during demyelination. Reduced neuronal MIF may increase neuronal vulnerability, whereas OPC-derived MIF supports remyelination.
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