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- W4313382169 abstract "Abstract Tumor necrosis factor-alpha (TNF) is a pleiotropic inflammatory cytokine that has been associated with the pathogenesis of several autoimmune diseases, including multiple sclerosis (MS). Consequently, TNF-blocking drugs have been widely used to treat many inflammatory conditions and have proven highly effective. However, treatment of MS patients with anti-TNF drugs leads to disease exacerbation and severe demyelination. This effect has been specifically associated with lack of TNF signaling through its receptor, TNFR2. However, the underlying mechanisms are not fully understood. Experimental autoimmune encephalomyelitis (EAE) is the most common animal model used to study MS. Our lab has recently generated TNFR2−/− DR2b+/+ mice to study the role of TNFR2 signaling in EAE in the context of the HLA-DR2b (DRB1*1501), a haplotype strongly associated with MS. We found that these mice developed progressive EAE characterized by increased demyelinating lesions. Strikingly, this phenotype was not due to lack of TNFR2 expression in T cells, but rather was associated with a decreased numbers of oligodendrocyte progenitor cells (OPCs) in the CNS. Moreover, we demonstrated that TNFR2 signaling is critical for expression of chemokines in the CNS, suggesting its involvement in OPC function and recruitment. Our studies provide key insights into CNS repair and regulatory mechanisms controlled by TNF during inflammation, and this information may help develop novel therapeutic strategies." @default.
- W4313382169 created "2023-01-06" @default.
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- W4313382169 date "2017-05-01" @default.
- W4313382169 modified "2023-10-18" @default.
- W4313382169 title "Signaling via TNFR2 mediates CNS remyelination in EAE through regulation of oligodendrocyte progenitor cells" @default.
- W4313382169 doi "https://doi.org/10.4049/jimmunol.198.supp.219.4" @default.
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