{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["19"],"submitter":["Paltser G"],"funding":["Canadian Institutes of Health Research"],"pubmed_abstract":["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"],"journal":["Molecular medicine (Cambridge, Mass.)"],"pagination":["149-59"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3745593"],"repository":["biostudies-literature"],"pubmed_title":["TRPV1 gates tissue access and sustains pathogenicity in autoimmune encephalitis."],"pmcid":["PMC3745593"],"pubmed_authors":["Maezawa Y","Paltser G","Sadovnick AD","Wu P","Ramagopalan SV","Laliberte CL","DeLuca GC","Astsaturov I","Winer S","Liu XJ","Tsui H","Henkelman RM","Cahill LS","Ebers GC","Dosch HM","Yantha J","Salter MW"],"additional_accession":[]},"is_claimable":false,"name":"TRPV1 gates tissue access and sustains pathogenicity in autoimmune encephalitis.","description":"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","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 Jul","modification":"2026-05-30T09:13:08.325Z","creation":"2025-07-28T03:03:54.628Z"},"accession":"S-EPMC3745593","cross_references":{"pubmed":["23689362"],"doi":["10.2119/molmed.2012.00329"]}}