{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Fujiwara M"],"funding":["National Multiple Sclerosis Society","NIAID NIH HHS","National Institute of Health","CSR NIH HHS"],"pagination":["103-13"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4420730"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["158(1)"],"pubmed_abstract":["The variable response to therapy in multiple sclerosis (MS) suggests a need for personalized approaches based on individual genetic differences. GWAS have linked CBLB gene polymorphisms with MS and recent evidence demonstrated that these polymorphisms can be associated with abnormalities in T cell function and response to interferon-β therapy. Cbl-b is an E3 ubiquitin ligase that regulates T cell activation and Cbl-b-deficient (Cbl-b(-/-)) mice show T cell abnormalities described in MS patients. We now show that Cbl-b(-/-) T cells demonstrate significant lymph node trafficking abnormalities. We thus asked whether the MS-approved drug, FTY720, postulated to trap T cells in lymphoid tissues, is less effective in the context of Cbl-b dysfunction. We now report that FTY720 significantly inhibi"],"journal":["Clinical immunology (Orlando, Fla.)"],"pubmed_title":["Cbl-b-deficient mice express alterations in trafficking-related molecules but retain sensitivity to the multiple sclerosis therapeutic agent, FTY720."],"pmcid":["PMC4420730"],"funding_grant_id":["AI097375","R01 AI097375","RG4070B7/2"],"pubmed_authors":["Anstadt EJ","Clark RB","Fujiwara M","Khanna KM"],"additional_accession":[]},"is_claimable":false,"name":"Cbl-b-deficient mice express alterations in trafficking-related molecules but retain sensitivity to the multiple sclerosis therapeutic agent, FTY720.","description":"The variable response to therapy in multiple sclerosis (MS) suggests a need for personalized approaches based on individual genetic differences. GWAS have linked CBLB gene polymorphisms with MS and recent evidence demonstrated that these polymorphisms can be associated with abnormalities in T cell function and response to interferon-β therapy. Cbl-b is an E3 ubiquitin ligase that regulates T cell activation and Cbl-b-deficient (Cbl-b(-/-)) mice show T cell abnormalities described in MS patients. We now show that Cbl-b(-/-) T cells demonstrate significant lymph node trafficking abnormalities. We thus asked whether the MS-approved drug, FTY720, postulated to trap T cells in lymphoid tissues, is less effective in the context of Cbl-b dysfunction. We now report that FTY720 significantly inhibi","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 May","modification":"2026-04-07T19:28:40.162Z","creation":"2019-03-27T01:51:03Z"},"accession":"S-EPMC4420730","cross_references":{"pubmed":["25829233"],"doi":["10.1016/j.clim.2015.03.018"]}}