{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang H"],"funding":["CAMS | Chinese Academy of Medical Sciences Initiative for Innovative Medicine ()","CAMS | Chinese Academy of Medical Sciences Initiative for Innovative Medicine","MOST | National Natural Science Foundation of China (NSFC)","Haihe Laboratory of Cell Ecosystem Innovation Fund","MOST | National Natural Science Foundation of China"],"pagination":["e2317658121"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10945852"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["121(11)"],"pubmed_abstract":["Identification of mechanisms that program early effector T cells to either terminal effector T (T<sub>eff</sub>) or memory T (T<sub>m</sub>) cells has important implications for protective immunity against infections and cancers. Here, we show that the cytosolic transcription factor aryl hydrocarbon receptor (AhR) is used by early T<sub>eff</sub> cells to program memory fate. Upon antigen engagement, AhR is rapidly up-regulated via reactive oxygen species signaling in early CD8<sup>+</sup> T<sub>eff</sub> cells, which does not affect the effector response, but is required for memory formation. Mechanistically, activated CD8<sup>+</sup> T cells up-regulate HIF-1α to compete with AhR for HIF-1β, leading to the loss of AhR activity in HIF-1α<sup>high</sup> short-lived effector cells, but sustained in HIF-1α<sup>low</sup> memory precursor effector cells (MPECs) with the help of autocrine IL-2. AhR then licenses CD8<sup>+</sup> MPECs in a quiescent state for memory formation. These findings partially resolve the long-standing issue of how T<sub>eff</sub> cells are regulated to differentiate into memory cells."],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Sustained AhR activity programs memory fate of early effector CD8<sup>+</sup> T cells."],"pmcid":["PMC10945852"],"funding_grant_id":["82271759","82388201","22HHXBSS00009","2021-I2M-1-021","32322030"],"pubmed_authors":["Liu J","Zhou N","Chen J","Zhang H","Zhou Y","Zhang Q","Lv J","Tang K","Yang Z","Li Y","Ma J","Luo X","Yuan W","Huang B"],"additional_accession":[]},"is_claimable":false,"name":"Sustained AhR activity programs memory fate of early effector CD8<sup>+</sup> T cells.","description":"Identification of mechanisms that program early effector T cells to either terminal effector T (T<sub>eff</sub>) or memory T (T<sub>m</sub>) cells has important implications for protective immunity against infections and cancers. Here, we show that the cytosolic transcription factor aryl hydrocarbon receptor (AhR) is used by early T<sub>eff</sub> cells to program memory fate. Upon antigen engagement, AhR is rapidly up-regulated via reactive oxygen species signaling in early CD8<sup>+</sup> T<sub>eff</sub> cells, which does not affect the effector response, but is required for memory formation. Mechanistically, activated CD8<sup>+</sup> T cells up-regulate HIF-1α to compete with AhR for HIF-1β, leading to the loss of AhR activity in HIF-1α<sup>high</sup> short-lived effector cells, but sustained in HIF-1α<sup>low</sup> memory precursor effector cells (MPECs) with the help of autocrine IL-2. AhR then licenses CD8<sup>+</sup> MPECs in a quiescent state for memory formation. These findings partially resolve the long-standing issue of how T<sub>eff</sub> cells are regulated to differentiate into memory cells.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Mar","modification":"2025-04-20T02:51:18.759Z","creation":"2025-02-19T03:10:04.45Z"},"accession":"S-EPMC10945852","cross_references":{"pubmed":["38437537"],"doi":["10.1073/pnas.2317658121"]}}