{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["McClory SE"],"funding":["NIAID NIH HHS","NCI NIH HHS"],"pubmed_abstract":["T cell exhaustion (T <sub>EX</sub> ) impairs the ability of T cells to clear chronic infection or cancer. While exhausted T cells are hypofunctional, some exhausted T cells retain effector gene signatures, a feature that is associated with expression of KLRs (killer lectin-like receptors). Although KLR <sup>+</sup> T cells may improve control of chronic antigen, the signaling molecules regulating this population are poorly understood. Using scRNA-seq, flow cytometry, RNA velocity, and scTCR-seq, we demonstrate that deleting the pseudokinase Trib1 shifts T <sub>EX</sub> towards CX3CR1 <sup>+</sup> intermediates (T <sub>INT</sub> ) with robust enrichment of KLR <sup>+</sup> CD8 <sup>+</sup> T cells (T <sub>KLR</sub> ) via clonal T cell expansion. These changes are associated with globally in"],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2023.02.16.528833"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9948998"],"repository":["biostudies-literature"],"pubmed_title":["The pseudokinase Trib1 regulates the transition of exhausted T cells to a KLR <sup>+</sup> CD8 <sup>+</sup> effector state and its deletion improves checkpoint blockade."],"pmcid":["PMC9948998"],"funding_grant_id":["R01 AI155577","P30 CA016520","T32 CA009140","P01 AI108545","P01 CA210944","U19 AI082630","T32 CA009615","R01 AI115712","R01 AI047833","K12 CA076931","U19 AI117950"],"pubmed_authors":["Xu L","Giles JR","Pear WS","Rome KS","Baxter AE","Wherry EJ","Bardhan O","Gimotty PA","Faryabi RB","Jordan MS","McClory SE"],"additional_accession":[]},"is_claimable":false,"name":"The pseudokinase Trib1 regulates the transition of exhausted T cells to a KLR <sup>+</sup> CD8 <sup>+</sup> effector state and its deletion improves checkpoint blockade.","description":"T cell exhaustion (T <sub>EX</sub> ) impairs the ability of T cells to clear chronic infection or cancer. While exhausted T cells are hypofunctional, some exhausted T cells retain effector gene signatures, a feature that is associated with expression of KLRs (killer lectin-like receptors). Although KLR <sup>+</sup> T cells may improve control of chronic antigen, the signaling molecules regulating this population are poorly understood. Using scRNA-seq, flow cytometry, RNA velocity, and scTCR-seq, we demonstrate that deleting the pseudokinase Trib1 shifts T <sub>EX</sub> towards CX3CR1 <sup>+</sup> intermediates (T <sub>INT</sub> ) with robust enrichment of KLR <sup>+</sup> CD8 <sup>+</sup> T cells (T <sub>KLR</sub> ) via clonal T cell expansion. These changes are associated with globally in","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2025-04-04T13:08:03.258Z","creation":"2025-04-04T13:08:03.258Z"},"accession":"S-EPMC9948998","cross_references":{"pubmed":["36824931"],"doi":["10.1101/2023.02.16.528833"]}}