<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-04-29T12:31:20Z</responseDate><request verb="GetRecord" identifier="oai:repisalud.isciii.es:20.500.12105/15107" metadataPrefix="marc">https://repisalud.isciii.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:repisalud.isciii.es:20.500.12105/15107</identifier><datestamp>2024-09-27T08:10:47Z</datestamp><setSpec>com_20.500.12105_19604</setSpec><setSpec>com_20.500.12105_2051</setSpec><setSpec>col_20.500.12105_19605</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Blanco-Domínguez, Rafael</subfield>
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      <subfield code="a">de la Fuente, Hortensia</subfield>
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      <subfield code="a">Rodríguez, Cristina</subfield>
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      <subfield code="a">Martín-Aguado, Laura</subfield>
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      <subfield code="a">Jiménez-Alejandre, Rosa</subfield>
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      <subfield code="a">Curtabbi, Andrea</subfield>
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      <subfield code="a">Garcia-Guimaraes, Marcos M</subfield>
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      <subfield code="a">Vera, Alberto</subfield>
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      <subfield code="a">Cuesta, Javier</subfield>
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      <subfield code="a">Bueno, Hector</subfield>
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      <subfield code="a">Villalba-Orero, María</subfield>
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      <subfield code="a">Enriquez, Jose Antonio</subfield>
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      <subfield code="a">Robson, Simon C</subfield>
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      <subfield code="a">Alfonso, Fernando</subfield>
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      <subfield code="a">Sánchez-Madrid, Francisco</subfield>
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      <subfield code="a">Martínez-González, José</subfield>
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      <subfield code="a">Martin, Pilar</subfield>
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      <subfield code="a">Garcia-Guimaraes, Marcos M.</subfield>
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      <subfield code="a">Robson, Simon C.</subfield>
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      <subfield code="c">2022-09-06</subfield>
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      <subfield code="a">Increasing evidences advocate for an important function of T cells in controlling immune homeostasis and pathogenesis after myocardial infarction (MI), although the underlying molecular mechanisms remain elusive. In this study, a broad analysis of immune markers in 283 patients revealed a significant CD69 overexpression on Treg cells after MI. Our results in mice showed that CD69 expression on Treg cells increased survival after left-anterior-descending coronary artery (LAD)-ligation. Cd69-/- mice developed strong IL-17+ γδT cell responses after ischemia that increased myocardial inflammation and, consequently, worsened cardiac function. CD69+ Treg cells, by induction of AhR-dependent CD39 ectonucleotidase activity, induced apoptosis and decreased IL-17A production in γδT cells. Adoptive transfer of CD69+ Treg cells to Cd69-/- mice after LAD-ligation reduced IL-17+ γδT cell recruitment, thus increasing survival. Consistently, clinical data from two independent cohorts of patients indicated that increased CD69 expression in peripheral blood cells after acute MI was associated with a lower risk of re-hospitalization for heart failure (HF) after 2.5 years of follow-up. This result remained significant after adjustment for age, sex and traditional cardiac damage biomarkers. Our data highlight CD69 expression on Treg cells as a potential prognostic factor and a therapeutic option to prevent HF after MI.</subfield>
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      <subfield code="a">J Clin Invest . 2022 Sep 6;e152418.</subfield>
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      <subfield code="a">10.1172/JCI152418</subfield>
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      <subfield code="a">1558-8238</subfield>
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      <subfield code="a">The Journal of clinical investigation</subfield>
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      <subfield code="a">http://hdl.handle.net/20.500.12105/15107</subfield>
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      <subfield code="a">CD69 expression on regulatory T cells protects from immune damage after myocardial infarction.</subfield>
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