| First Author | Paltser G | Year | 2013 |
| Journal | Mol Med | Volume | 19 |
| Pages | 149-59 | PubMed ID | 23689362 |
| Mgi Jnum | J:315286 | Mgi Id | MGI:6830011 |
| Doi | 10.2119/molmed.2012.00329 | Citation | Paltser G, et al. (2013) TRPV1 gates tissue access and sustains pathogenicity in autoimmune encephalitis. Mol Med 19:149-59 |
| abstractText | Multiple sclerosis (MS) is a chronic progressive, demyelinating condition whose therapeutic needs are unmet, and whose pathoetiology is elusive. We report that transient receptor potential vanilloid-1 (TRPV1) expressed in a major sensory neuron subset, controls severity and progression of experimental autoimmune encephalomyelitis (EAE) in mice and likely in primary progressive MS. TRPV1-/- B6 congenics are protected from EAE. Increased survival reflects reduced central nervous systems (CNS) infiltration, despite indistinguishable T cell autoreactivity and pathogenicity in the periphery of TRPV1-sufficient and -deficient mice. The TRPV1+ neurovascular complex defining the blood-CNS barriers promoted invasion of pathogenic lymphocytes without the contribution of TRPV1-dependent neuropeptides such as substance P. In MS patients, we found a selective risk-association of the missense rs877610 TRPV1 single nucleotide polymorphism (SNP) in primary progressive disease. Our findings indicate that TRPV1 is a critical disease modifier in EAE, and we identify a predictor of severe disease course and a novel target for MS therapy. |
