{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gao J"],"funding":["National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["2077"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12949000"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(1)"],"pubmed_abstract":["Chimeric antigen receptor macrophages (CAR-Ms) therapy has shown great promise in liver fibrosis, however limited anti-inflammatory capacity of CAR-Ms in the fibrotic foci compromises their anti-fibrotic potency. We here report tripartite motif containing 13 (TRIM13) engineered CAR-Ms for effectively manipulating the anti-inflammatory phenotype of CAR-Ms, augmenting their anti-fibrosis efficacy. Specifically, our efferocytosis-sparked lipid nanoparticles (ESLNPs) efficiently engineered fibrosis-associated macrophages to anti-inflammatory CAR-Ms by co-delivering mRNA encoding TRIM13 and anti-fibroblast activation protein (FAP) CAR respectively. Our data demonstrated these reprogrammed CAR-Ms exhibited a sustained anti-inflammatory phenotype via blocking the mitochondrial DNA (mtDNA)-STING p"],"journal":["Nature communications"],"pubmed_title":["TRIM13 in situ engineering boosts anti-inflammatory capacity of CAR-Ms for liver fibrosis therapy."],"pmcid":["PMC12949000"],"funding_grant_id":["82350125，82425056，82173763"],"pubmed_authors":["Li C","Dong X","Shao L","Bo L","Han M","Tang C","Fu Z","Gao J","Chen C","Zhao X","Li N","Yang Z","Li Y","Li T","Jiang X","Dai K","Zhao K","Song Y"],"additional_accession":[]},"is_claimable":false,"name":"TRIM13 in situ engineering boosts anti-inflammatory capacity of CAR-Ms for liver fibrosis therapy.","description":"Chimeric antigen receptor macrophages (CAR-Ms) therapy has shown great promise in liver fibrosis, however limited anti-inflammatory capacity of CAR-Ms in the fibrotic foci compromises their anti-fibrotic potency. We here report tripartite motif containing 13 (TRIM13) engineered CAR-Ms for effectively manipulating the anti-inflammatory phenotype of CAR-Ms, augmenting their anti-fibrosis efficacy. Specifically, our efferocytosis-sparked lipid nanoparticles (ESLNPs) efficiently engineered fibrosis-associated macrophages to anti-inflammatory CAR-Ms by co-delivering mRNA encoding TRIM13 and anti-fibroblast activation protein (FAP) CAR respectively. Our data demonstrated these reprogrammed CAR-Ms exhibited a sustained anti-inflammatory phenotype via blocking the mitochondrial DNA (mtDNA)-STING p","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Feb","modification":"2026-07-16T23:15:31.524Z","creation":"2026-07-12T03:11:10.024Z"},"accession":"S-EPMC12949000","cross_references":{"pubmed":["41760658"],"doi":["10.1038/s41467-026-69858-3"]}}