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]. The gene discussed is TNFRSF1B; the disease is experimental autoimmune encephalomyelitis.