In support of this, TNFR2 activation on microglia promotes the induction of anti-inflammatory pathways, and TNFR2 ablation in microglia led to the early onset of experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis, with increased leukocyte infiltration, T cell activation, and demyelination [53,54]. This evidence concerns the gene TNFRSF1B and multiple sclerosis.