{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Nagashima H"],"funding":["NIAID NIH HHS"],"pagination":["449-56"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4108451"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(5)"],"pubmed_abstract":["The physiological functions of members of the tumor-necrosis factor (TNF) receptor (TNFR)-associated factor (TRAF) family in T cell immunity are not well understood. We found that in the presence of interleukin 6 (IL-6), naive TRAF5-deficient CD4(+) T cells showed an enhanced ability to differentiate into the TH17 subset of helper T cells. Accordingly, TH17 cell-associated experimental autoimmune encephalomyelitis (EAE) was greatly exaggerated in Traf5(-/-) mice. Although it is normally linked with TNFR signaling pathways, TRAF5 constitutively associated with a cytoplasmic region in the signal-transducing receptor gp130 that overlaps with the binding site for the transcription activator STAT3 and suppressed the recruitment and activation of STAT3 in response to IL-6. Our results identify T"],"journal":["Nature immunology"],"pubmed_title":["The adaptor TRAF5 limits the differentiation of inflammatory CD4(+) T cells by antagonizing signaling via the receptor for IL-6."],"pmcid":["PMC4108451"],"funding_grant_id":["AI049453","R01 AI049453"],"pubmed_authors":["Yamaki S","Ishii N","Okuyama Y","So T","Nakano H","Asao A","Kawabe T","Croft M","Nagashima H"],"additional_accession":[]},"is_claimable":false,"name":"The adaptor TRAF5 limits the differentiation of inflammatory CD4(+) T cells by antagonizing signaling via the receptor for IL-6.","description":"The physiological functions of members of the tumor-necrosis factor (TNF) receptor (TNFR)-associated factor (TRAF) family in T cell immunity are not well understood. We found that in the presence of interleukin 6 (IL-6), naive TRAF5-deficient CD4(+) T cells showed an enhanced ability to differentiate into the TH17 subset of helper T cells. Accordingly, TH17 cell-associated experimental autoimmune encephalomyelitis (EAE) was greatly exaggerated in Traf5(-/-) mice. Although it is normally linked with TNFR signaling pathways, TRAF5 constitutively associated with a cytoplasmic region in the signal-transducing receptor gp130 that overlaps with the binding site for the transcription activator STAT3 and suppressed the recruitment and activation of STAT3 in response to IL-6. Our results identify T","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 May","modification":"2025-04-26T08:34:22.265Z","creation":"2019-03-27T01:32:38Z"},"accession":"S-EPMC4108451","cross_references":{"pubmed":["24681564"],"doi":["10.1038/ni.2863"]}}