{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Warunek JJ"],"funding":["NIBIB NIH HHS","NIAID NIH HHS","NHLBI NIH HHS","NCI NIH HHS","American Society of Transplantation","National Institutes of Health","NIAMS NIH HHS"],"pagination":["e173593"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11601918"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["134(23)"],"pubmed_abstract":["Chronic rejection (CR) after organ transplantation is alloimmune injury manifested by graft vascular remodeling and fibrosis that is resistant to immunosuppression. Single-cell RNA-Seq analysis of MHC class II-mismatched (MHCII-mismatched) heart transplants developing chronic rejection identified graft IL-33 as a stimulator of tissue repair pathways in infiltrating macrophages and Tregs. Using IL-33-deficient donor mice, we show that graft fibroblast-derived IL-33 potently induced amphiregulin (Areg) expression by recipient Tregs. The assessment of clinical samples also confirmed increased expression of Areg by intragraft Tregs also during rejection. Areg is an EGF secreted by multiple immune cells to shape immunomodulation and tissue repair. In particular, Areg is proposed to play a major"],"journal":["The Journal of clinical investigation"],"pubmed_title":["Dysregulated Treg repair responses lead to chronic rejection after heart transplantation."],"pmcid":["PMC11601918"],"funding_grant_id":["R01AR073527","R01HL22489","R56AI139327","F31 HL170514","T32 AI074490","T32EB001026","F30AI147437","U01AI077867","U01 AI077867","T32CA082084","R56 AI139327","F30 AI147437","R01 AR073527","T32 CA082084","F31HL170514","998676","5T32AI074490-14","R01 HL122489","T32 EB001026"],"pubmed_authors":["Warunek JJ","Turnquist HR","Dwyer GK","Demetris AJ","Tabib T","Ross MA","Baron K","Lafyatis R","Webber SA","Abou-Daya KI","Wood-Trageser MA","Spencer H","Leon Colon E","Li T","Watkins SC","Wang S","Fan L","Zhang X","Sanders SM","Bou Saba J","Mathews LR","Traczek S","Lesniak A"],"additional_accession":[]},"is_claimable":false,"name":"Dysregulated Treg repair responses lead to chronic rejection after heart transplantation.","description":"Chronic rejection (CR) after organ transplantation is alloimmune injury manifested by graft vascular remodeling and fibrosis that is resistant to immunosuppression. Single-cell RNA-Seq analysis of MHC class II-mismatched (MHCII-mismatched) heart transplants developing chronic rejection identified graft IL-33 as a stimulator of tissue repair pathways in infiltrating macrophages and Tregs. Using IL-33-deficient donor mice, we show that graft fibroblast-derived IL-33 potently induced amphiregulin (Areg) expression by recipient Tregs. The assessment of clinical samples also confirmed increased expression of Areg by intragraft Tregs also during rejection. Areg is an EGF secreted by multiple immune cells to shape immunomodulation and tissue repair. In particular, Areg is proposed to play a major","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Dec","modification":"2026-06-03T05:30:47.252Z","creation":"2026-04-24T03:14:40.675Z"},"accession":"S-EPMC11601918","cross_references":{"pubmed":["39621314"],"doi":["10.1172/JCI173593"]}}