<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Miller ML</submitter><funding>American Heart Association</funding><funding>HHS | National Institutes of Health</funding><funding>NICHD NIH HHS</funding><funding>Howard Hughes Medical Institute</funding><funding>NIAID NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>HHS | NIH | National Heart, Lung, and Blood Institute</funding><funding>HHS | NIH | National Institute of Allergy and Infectious Diseases</funding><pagination>23682-23690</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6876241</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>116(47)</volume><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 &lt;i>Listeria monocytogenes&lt;/i> (Lm) months after transplantation can erode or transiently abrogate established tolerance. I</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>Resilience of T cell-intrinsic dysfunction in transplantation tolerance.</pubmed_title><pmcid>PMC6876241</pmcid><funding_grant_id>T32 HL07237</funding_grant_id><funding_grant_id>P01AI-97113</funding_grant_id><funding_grant_id>T32 HL007237</funding_grant_id><funding_grant_id>P01 AI097113</funding_grant_id><funding_grant_id>56006772</funding_grant_id><funding_grant_id>T32 HD007009</funding_grant_id><funding_grant_id>15PRE22180007</funding_grant_id><funding_grant_id>13PRE14550022</funding_grant_id><pubmed_authors>Mora Solano C</pubmed_authors><pubmed_authors>Chong AS</pubmed_authors><pubmed_authors>Wang P</pubmed_authors><pubmed_authors>Alegre ML</pubmed_authors><pubmed_authors>Miller ML</pubmed_authors><pubmed_authors>Chen L</pubmed_authors><pubmed_authors>McIntosh CM</pubmed_authors><pubmed_authors>Watkins E</pubmed_authors><pubmed_authors>Lei YM</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Daniels MD</pubmed_authors></additional><is_claimable>false</is_claimable><name>Resilience of T cell-intrinsic dysfunction in transplantation tolerance.</name><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 &lt;i>Listeria monocytogenes&lt;/i> (Lm) months after transplantation can erode or transiently abrogate established tolerance. I</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Nov</publication><modification>2025-05-31T23:02:43.121Z</modification><creation>2025-05-31T23:02:43.121Z</creation></dates><accession>S-EPMC6876241</accession><cross_references><pubmed>31685610</pubmed><doi>10.1073/pnas.1910298116</doi></cross_references></HashMap>