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dc.contributor.authorAghajanian, Haig
dc.contributor.authorKimura, Toru
dc.contributor.authorRurik, Joel G
dc.contributor.authorHancock, Aidan S
dc.contributor.authorLeibowitz, Michael S
dc.contributor.authorLi, Li
dc.contributor.authorScholler, John
dc.contributor.authorMonslow, James
dc.contributor.authorLo, Albert
dc.contributor.authorHan, Wei
dc.contributor.authorWang, Tao
dc.contributor.authorBedi, Kenneth
dc.contributor.authorMorley, Michael P
dc.contributor.authorLinares Saldana, Ricardo A
dc.contributor.authorBolar, Nikhita A
dc.contributor.authorMcDaid, Kendra
dc.contributor.authorAssenmacher, Charles-Antoine
dc.contributor.authorSmith, Cheryl L
dc.contributor.authorWirth, Dagmar
dc.contributor.authorJune, Carl H
dc.contributor.authorMargulies, Kenneth B
dc.contributor.authorJain, Rajan
dc.contributor.authorPuré, Ellen
dc.contributor.authorAlbelda, Steven M
dc.contributor.authorEpstein, Jonathan A
dc.date.accessioned2020-08-18T09:28:42Z
dc.date.available2020-08-18T09:28:42Z
dc.date.issued2019-09-11
dc.identifier.citationNature. 2019;573(7774):430-433. doi:10.1038/s41586-019-1546-z.en_US
dc.identifier.pmid31511695
dc.identifier.doi10.1038/s41586-019-1546-z
dc.identifier.urihttp://hdl.handle.net/10033/622412
dc.description.abstractFibrosis is observed in nearly every form of myocardial disease1. Upon injury, cardiac fibroblasts in the heart begin to remodel the myocardium by depositing excess extracellular matrix, resulting in increased stiffness and reduced compliance of the tissue. Excessive cardiac fibrosis is an important factor in the progression of various forms of cardiac disease and heart failure2. However, clinical interventions and therapies that target fibrosis remain limited3. Here we demonstrate the efficacy of redirected T cell immunotherapy to specifically target pathological cardiac fibrosis in mice. We find that cardiac fibroblasts that express a xenogeneic antigen can be effectively targeted and ablated by adoptive transfer of antigen-specific CD8+ T cells. Through expression analysis of the gene signatures of cardiac fibroblasts obtained from healthy and diseased human hearts, we identify an endogenous target of cardiac fibroblasts-fibroblast activation protein. Adoptive transfer of T cells that express a chimeric antigen receptor against fibroblast activation protein results in a significant reduction in cardiac fibrosis and restoration of function after injury in mice. These results provide proof-of-principle for the development of immunotherapeutic drugs for the treatment of cardiac disease.en_US
dc.language.isoenen_US
dc.publisherNature publishing group(NPG)en_US
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6752964/en_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleTargeting cardiac fibrosis with engineered T cells.en_US
dc.typeArticleen_US
dc.typeOtheren_US
dc.identifier.eissn1476-4687
dc.contributor.departmentHZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.en_US
dc.identifier.journalNatureen_US
dc.identifier.pmcidPMC6752964
dc.source.volume573
dc.source.issue7774
dc.source.beginpage430
dc.source.endpage433
refterms.dateFOA2020-08-18T09:28:43Z
dc.source.journaltitleNature
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryEngland


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