GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE339nnn/GSE339077/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE339077GEOGSEfalseFibronectin inhibition restores myelination in endothelial TNFR2-depedent non-remitting Experimental Autoimmune Encephalomyelitis [RNA-seq]Multiple Sclerosis (MS) is characterized by impaired remyelination and progressive neurodegeneration. Here, we investigated the mechanisms underlying remyelination failure in Experimental Autoimmune Encephalomyelitis (EAE), a murine model of MS. Tumor Necrosis Factor Receptor 2 (TNFR2) deletion causes a severe non-remitting disease after EAE induction. To delineate the TNFR2-dependent effect on remyelination, we assessed the transcriptional profiles of mice expressing TNFR2 (TNFR2FF) and TNFR2-deleted mice (TNFR2KO) at key EAE stages. Our study highlights the key role of TNFR2 at the non-remitting stage of the disease.2026/09/07GSE339077GSM9888093GSM9888094GSM9888091GSM9888092GSM9888097GSM9888086GSM9888087GSM9888098GSM9888095GSM9888096GSM9888085GSM9888090GSM9888099GSM9888088GSM9888100GSM988808916331339077Mus musculus