{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tili E"],"funding":["HHS | NIH | National Cancer Institute","CLL Global Research Foundation","NCI NIH HHS","CLL Global Research Foundation (CLLGRF)","HHS | NIH | National Cancer Institute (NCI)"],"pagination":["e2408649121"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11260163"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["121(29)"],"pubmed_abstract":["Elevated levels of <i>miR-155</i> in solid and liquid malignancies correlate with aggressiveness of the disease. In this manuscript, we show that <i>miR-155</i> targets transcripts encoding IcosL, the ligand for Inducible T-cell costimulator (Icos), thus impairing the ability of T cells to recognize and eliminate malignant cells. We specifically found that overexpression of <i>miR-155</i> in B cells of Eµ-<i>miR-155</i> mice causes loss of IcosL expression as they progress toward malignancy. Similarly, in mice where <i>miR-155</i> expression is controlled by a Cre-Tet-OFF system, <i>miR-155</i> induction led to malignant infiltrates lacking <i>IcosL</i> expression. Conversely, turning <i>miR-155</i> OFF led to tumor regression and emergence of infiltrates composed of IcosL-positive B cells"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["<i>MiR-155</i>-targeted IcosL controls tumor rejection."],"pmcid":["PMC11260163"],"funding_grant_id":["AWD-115284","P30 CA016058","AWD-116510","P30CA016058"],"pubmed_authors":["Nuovo GJ","Tili E","Otsu H","Palamarchuk A","Croce CM","Balatti V","Commisso TL","Michaille JJ"],"additional_accession":[]},"is_claimable":false,"name":"<i>MiR-155</i>-targeted IcosL controls tumor rejection.","description":"Elevated levels of <i>miR-155</i> in solid and liquid malignancies correlate with aggressiveness of the disease. In this manuscript, we show that <i>miR-155</i> targets transcripts encoding IcosL, the ligand for Inducible T-cell costimulator (Icos), thus impairing the ability of T cells to recognize and eliminate malignant cells. We specifically found that overexpression of <i>miR-155</i> in B cells of Eµ-<i>miR-155</i> mice causes loss of IcosL expression as they progress toward malignancy. Similarly, in mice where <i>miR-155</i> expression is controlled by a Cre-Tet-OFF system, <i>miR-155</i> induction led to malignant infiltrates lacking <i>IcosL</i> expression. Conversely, turning <i>miR-155</i> OFF led to tumor regression and emergence of infiltrates composed of IcosL-positive B cells","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2026-06-02T00:09:42.249Z","creation":"2026-05-24T03:07:39.566Z"},"accession":"S-EPMC11260163","cross_references":{"pubmed":["38980909"],"doi":["10.1073/pnas.2408649121"]}}