 The study reports that transient receptor-potential vanyloid 1, TRPV1, expressed in major sensory neuron subset controls severity and progression of experimental autoimmune encephalomyelitis, EAE, in mice, and likely in primary progressive MIS-TRPV1. Deficient B6 congenics are protected from EAE due to reduced central nervous systems, CNS, infiltration, despite indistinguishable T-cell auto-reactivity and pathogenicity in the periphery of TRPV1, sufficient and deficient mice. The study identifies a predictor of severe disease cause and a novel target for MS therapy. This article was authored by Jeffrey Paltzer, Xue Zhenliu, Jason Yanfa, and others.