{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Meylan F"],"funding":["Intramural NIH HHS","Medical Research Council"],"pagination":["79-89"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2760084"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["29(1)"],"pubmed_abstract":["DR3 (TRAMP, LARD, WSL-1, TNFRSF25) is a death-domain-containing tumor necrosis factor (TNF)-family receptor primarily expressed on T cells. TL1A, the TNF-family ligand for DR3, can costimulate T cells, but the physiological function of TL1A-DR3 interactions in immune responses is not known. Using DR3-deficient mice, we identified DR3 as the receptor responsible for TL1A-induced T cell costimulation and dendritic cells as the likely source for TL1A during T cell activation. Despite its role in costimulation, DR3 was not required for in vivo T cell priming, for polarization into T helper 1 (Th1), Th2, or Th17 effector cell subtypes, or for effective control of infection with Toxoplasma gondii. Instead, DR3 expression was required on T cells for immunopathology, local T cell accumulation, and"],"journal":["Immunity"],"pubmed_title":["The TNF-family receptor DR3 is essential for diverse T cell-mediated inflammatory diseases."],"pmcid":["PMC2760084"],"funding_grant_id":["G0300180(65735)","G0500617(74644)","G0500617","Z01 AR041174-01","G0300180"],"pubmed_authors":["Kinder M","Bundoc V","Shevach EM","Davidson TS","Kahle E","Meylan F","Jankovic D","Siegel RM","Wang EC","Acharya K","Hodges M","Keane-Myers A"],"additional_accession":[]},"is_claimable":false,"name":"The TNF-family receptor DR3 is essential for diverse T cell-mediated inflammatory diseases.","description":"DR3 (TRAMP, LARD, WSL-1, TNFRSF25) is a death-domain-containing tumor necrosis factor (TNF)-family receptor primarily expressed on T cells. TL1A, the TNF-family ligand for DR3, can costimulate T cells, but the physiological function of TL1A-DR3 interactions in immune responses is not known. Using DR3-deficient mice, we identified DR3 as the receptor responsible for TL1A-induced T cell costimulation and dendritic cells as the likely source for TL1A during T cell activation. Despite its role in costimulation, DR3 was not required for in vivo T cell priming, for polarization into T helper 1 (Th1), Th2, or Th17 effector cell subtypes, or for effective control of infection with Toxoplasma gondii. Instead, DR3 expression was required on T cells for immunopathology, local T cell accumulation, and","dates":{"release":"2008-01-01T00:00:00Z","publication":"2008 Jul","modification":"2025-04-03T23:19:02.408Z","creation":"2019-03-27T00:25:46Z"},"accession":"S-EPMC2760084","cross_references":{"pubmed":["18571443"],"doi":["10.1016/j.immuni.2008.04.021"]}}