{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Miller ML"],"funding":["American Heart Association","HHS | National Institutes of Health","NICHD NIH HHS","Howard Hughes Medical Institute","NIAID NIH HHS","NHLBI NIH HHS","HHS | NIH | National Heart, Lung, and Blood Institute","HHS | NIH | National Institute of Allergy and Infectious Diseases"],"pagination":["23682-23690"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6876241"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["116(47)"],"pubmed_abstract":["Following antigen stimulation, naïve T cells differentiate into memory cells that mediate antigen clearance more efficiently upon repeat encounter. Donor-specific tolerance can be achieved in a subset of transplant recipients, but some of these grafts are rejected after years of stability, often following infections. Whether T cell memory can develop from a tolerant state and whether these formerly tolerant patients develop antidonor memory is not known. Using a mouse model of cardiac transplantation in which donor-specific tolerance is induced with costimulation blockade (CoB) plus donor-specific transfusion (DST), we have previously shown that systemic infection with <i>Listeria monocytogenes</i> (Lm) months after transplantation can erode or transiently abrogate established tolerance. I"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Resilience of T cell-intrinsic dysfunction in transplantation tolerance."],"pmcid":["PMC6876241"],"funding_grant_id":["T32 HL07237","P01AI-97113","T32 HL007237","P01 AI097113","56006772","T32 HD007009","15PRE22180007","13PRE14550022"],"pubmed_authors":["Mora Solano C","Chong AS","Wang P","Alegre ML","Miller ML","Chen L","McIntosh CM","Watkins E","Lei YM","Wang Y","Daniels MD"],"additional_accession":[]},"is_claimable":false,"name":"Resilience of T cell-intrinsic dysfunction in transplantation tolerance.","description":"Following antigen stimulation, naïve T cells differentiate into memory cells that mediate antigen clearance more efficiently upon repeat encounter. Donor-specific tolerance can be achieved in a subset of transplant recipients, but some of these grafts are rejected after years of stability, often following infections. Whether T cell memory can develop from a tolerant state and whether these formerly tolerant patients develop antidonor memory is not known. Using a mouse model of cardiac transplantation in which donor-specific tolerance is induced with costimulation blockade (CoB) plus donor-specific transfusion (DST), we have previously shown that systemic infection with <i>Listeria monocytogenes</i> (Lm) months after transplantation can erode or transiently abrogate established tolerance. I","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Nov","modification":"2025-05-31T23:02:43.121Z","creation":"2025-05-31T23:02:43.121Z"},"accession":"S-EPMC6876241","cross_references":{"pubmed":["31685610"],"doi":["10.1073/pnas.1910298116"]}}