{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Duan X"],"funding":["Shenzhen Municipal Science and Technology Innovation Council | Shenzhen Science and Technology Innovation Program","GDSTC | Basic and Applied Basic Research Foundation of Guangdong Province","Guangdong Provincial Key Laboratory of Construction Foundation ()","Guangdong Provincial Key Laboratory of Construction Foundation","MOST | National Natural Science Foundation of China (NSFC)","the Science and Technology Planning Project of Guangzhou","Scientific Research start up Project of Zhuhai People&apos;s Hospital","GDSTC | Basic and Applied Basic Research Foundation of Guangdong Province ()","Scientific Research start up Project of Zhuhai People's Hospital","Shenzhen Municipal Science and Technology Innovation Council | Shenzhen Science and Technology Innovation Program ()","MOST | National Natural Science Foundation of China"],"pagination":["3005-3025"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11555380"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(11)"],"pubmed_abstract":["Retinoic acid-inducible gene I (RIG-I) is a pattern recognition receptor involved in innate immunity, but its role in adaptive immunity, specifically in the context of CD8<sup>+</sup> T-cell antitumour immunity, remains unclear. Here, we demonstrate that RIG-I is upregulated in tumour-infiltrating CD8<sup>+</sup> T cells, where it functions as an intracellular checkpoint to negatively regulate CD8<sup>+</sup> T-cell function and limit antitumour immunity. Mechanistically, the upregulation of RIG-I in CD8<sup>+</sup> T cells is induced by activated T cells, and directly inhibits the AKT/glycolysis signalling pathway. In addition, knocking out RIG-I enhances the efficacy of adoptively transferred T cells against solid tumours, and inhibiting RIG-I enhances the response to PD-1 blockade. Over"],"journal":["EMBO molecular medicine"],"pubmed_title":["RIG-I is an intracellular checkpoint that limits CD8<sup>+</sup> T-cell antitumour immunity."],"pmcid":["PMC11555380"],"funding_grant_id":["2020A1515110013","82304589","82103433","32200936","32470961","2021A1515220187","82103306","82230067","2021A1515110561","JCYJ20220818101808018","2024A1515012563","8204415","2021B1212040004","SL2024A03J00598","2021KYQD-04"],"pubmed_authors":["Zhang G","Yi Z","Lin Q","Liang X","Lei H","Sun HW","Lin X","Liu S","Meng Y","Zhao X","Liu Y","Zhan M","Liang H","Chen X","Wu Y","Yang G","Yang M","Sun T","Li W","Lu L","Yang Z","Li Z","Feng J","Diao W","Hu J","Zhang Y","Li XY","Liu D","Duan X"],"additional_accession":[]},"is_claimable":false,"name":"RIG-I is an intracellular checkpoint that limits CD8<sup>+</sup> T-cell antitumour immunity.","description":"Retinoic acid-inducible gene I (RIG-I) is a pattern recognition receptor involved in innate immunity, but its role in adaptive immunity, specifically in the context of CD8<sup>+</sup> T-cell antitumour immunity, remains unclear. Here, we demonstrate that RIG-I is upregulated in tumour-infiltrating CD8<sup>+</sup> T cells, where it functions as an intracellular checkpoint to negatively regulate CD8<sup>+</sup> T-cell function and limit antitumour immunity. Mechanistically, the upregulation of RIG-I in CD8<sup>+</sup> T cells is induced by activated T cells, and directly inhibits the AKT/glycolysis signalling pathway. In addition, knocking out RIG-I enhances the efficacy of adoptively transferred T cells against solid tumours, and inhibiting RIG-I enhances the response to PD-1 blockade. Over","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2026-07-16T18:41:20.01Z","creation":"2025-04-06T10:14:28.013Z"},"accession":"S-EPMC11555380","cross_references":{"pubmed":["39322862"],"doi":["10.1038/s44321-024-00136-9"]}}