{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Simula L"],"funding":["Associazione Italiana per la Ricerca sul Cancro","Fondazione Italiana Sclerosi Multipla"],"pagination":["188-205"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8732338"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_abstract":["Programmed cell death-1 (PD-1) signaling downregulates the T-cell response, promoting an exhausted state in tumor-infiltrating T cells, through mostly unveiled molecular mechanisms. Dynamin-related protein-1 (Drp1)-dependent mitochondrial fission plays a crucial role in sustaining T-cell motility, proliferation, survival, and glycolytic engagement. Interestingly, such processes are exactly those inhibited by PD-1 in tumor-infiltrating T cells. Here, we show that PD-1<sup>pos</sup> CD8<sup>+</sup> T cells infiltrating an MC38 (murine adenocarcinoma)-derived murine tumor mass have a downregulated Drp1 activity and more elongated mitochondria compared with PD-1<sup>neg</sup> counterparts. Also, PD-1<sup>pos</sup> lymphocytic elements infiltrating a human colon cancer rarely express active Drp"],"journal":["Molecular oncology"],"pubmed_title":["PD-1-induced T cell exhaustion is controlled by a Drp1-dependent mechanism."],"pmcid":["PMC8732338"],"funding_grant_id":["2018/S/5","IG‐2017 19826","2016/R/18"],"pubmed_authors":["Campello S","Scarpelli G","Colamatteo A","Cancila V","De Angelis B","Antonucci Y","Quintarelli C","Matarese G","Tripodo C","Simula L","Procaccini C","Manni S"],"additional_accession":[]},"is_claimable":false,"name":"PD-1-induced T cell exhaustion is controlled by a Drp1-dependent mechanism.","description":"Programmed cell death-1 (PD-1) signaling downregulates the T-cell response, promoting an exhausted state in tumor-infiltrating T cells, through mostly unveiled molecular mechanisms. Dynamin-related protein-1 (Drp1)-dependent mitochondrial fission plays a crucial role in sustaining T-cell motility, proliferation, survival, and glycolytic engagement. Interestingly, such processes are exactly those inhibited by PD-1 in tumor-infiltrating T cells. Here, we show that PD-1<sup>pos</sup> CD8<sup>+</sup> T cells infiltrating an MC38 (murine adenocarcinoma)-derived murine tumor mass have a downregulated Drp1 activity and more elongated mitochondria compared with PD-1<sup>neg</sup> counterparts. Also, PD-1<sup>pos</sup> lymphocytic elements infiltrating a human colon cancer rarely express active Drp","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jan","modification":"2025-04-18T17:09:31.385Z","creation":"2022-02-11T15:08:22.969Z"},"accession":"S-EPMC8732338","cross_references":{"pubmed":["34535949"],"doi":["10.1002/1878-0261.13103"]}}