{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,31]],"date-time":"2026-10-31T02:14:34Z","timestamp":1793412874500,"version":"4.5.0"},"reference-count":49,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circ: Heart Failure"],"published-print":{"date-parts":[[2017,3]]},"abstract":"<jats:sec>\n                    <jats:title>Background\u2014<\/jats:title>\n                    <jats:p>Inappropriately sustained inflammation is a hallmark of chronic ischemic heart failure (HF); however, the pathophysiological role of T lymphocytes is unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and Results\u2014<\/jats:title>\n                    <jats:p>\n                      Permanent coronary ligation was performed in adult C57BL\/6 mice. When compared with sham-operated mice, mice with HF (8 weeks after ligation) exhibited the following features: (1) significant (\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.05) expansion of circulating CD3\n                      <jats:sup>+<\/jats:sup>\n                      CD8\n                      <jats:sup>+<\/jats:sup>\n                      cytotoxic and CD3\n                      <jats:sup>+<\/jats:sup>\n                      CD4\n                      <jats:sup>+<\/jats:sup>\n                      helper (Th) T lymphocytes, together with increased Th1, Th2, Th17, and regulatory T-cell (Treg) CD4\n                      <jats:sup>+<\/jats:sup>\n                      subsets; (2) significant expansion of CD8\n                      <jats:sup>+<\/jats:sup>\n                      and CD4\n                      <jats:sup>+<\/jats:sup>\n                      T cells in failing myocardium, with increased Th1, Th2, Th17, and Treg CD4\n                      <jats:sup>+<\/jats:sup>\n                      subsets, marked reduction of the Th1\/Th2 ratio, augmentation of the Th17\/Treg ratio, and upregulation of Th2 cytokines; and (3) significantly increased Th1, Th2, Th17 cells, and Tregs, in the spleen and mediastinal lymph nodes, with expansion of splenic antigen-experienced effector and memory CD4\n                      <jats:sup>+<\/jats:sup>\n                      T cells. Antibody-mediated CD4\n                      <jats:sup>+<\/jats:sup>\n                      T-cell depletion in HF mice (starting 4 weeks after ligation) reduced cardiac infiltration of CD4\n                      <jats:sup>+<\/jats:sup>\n                      T cells and prevented progressive left ventricular dilatation and hypertrophy, whereas adoptive transfer of splenic CD4\n                      <jats:sup>+<\/jats:sup>\n                      T cells (and, to a lesser extent, cardiac CD3\n                      <jats:sup>+<\/jats:sup>\n                      T cells) from donor mice with HF induced long-term left ventricular dysfunction, fibrosis, and hypertrophy in naive recipient mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions\u2014<\/jats:title>\n                    <jats:p>\n                      CD4\n                      <jats:sup>+<\/jats:sup>\n                      T lymphocytes are globally expanded and activated in chronic ischemic HF, with Th2 (versus Th1) and Th17 (versus Treg) predominance in failing hearts, and with expansion of memory T cells in the spleen. Cardiac and splenic T cells in HF are primed to induce cardiac injury and remodeling, and retain this memory on adoptive transfer.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circheartfailure.116.003688","type":"journal-article","created":{"date-parts":[[2017,2,27]],"date-time":"2017-02-27T21:00:26Z","timestamp":1488229226000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":298,"title":["Activated T Lymphocytes are Essential Drivers of Pathological Remodeling in Ischemic Heart Failure"],"prefix":"10.1161","volume":"10","author":[{"given":"Shyam S.","family":"Bansal","sequence":"first","affiliation":[{"name":"From the Division of Cardiovascular Disease, Comprehensive Cardiovascular Center, University of Alabama at Birmingham (S.S.B., M.A.I., M.G., B.P., T.H., S.D.P.); and Medical Service, Birmingham Veterans Administration Medical Center, AL (S.S.B., S.D.P.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohamed Ameen","family":"Ismahil","sequence":"additional","affiliation":[{"name":"From the Division of Cardiovascular Disease, Comprehensive Cardiovascular Center, University of Alabama at Birmingham (S.S.B., M.A.I., M.G., B.P., T.H., S.D.P.); and Medical Service, Birmingham Veterans Administration Medical Center, AL (S.S.B., S.D.P.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mehak","family":"Goel","sequence":"additional","affiliation":[{"name":"From the Division of Cardiovascular Disease, Comprehensive Cardiovascular Center, University of Alabama at Birmingham (S.S.B., M.A.I., M.G., B.P., T.H., S.D.P.); and Medical Service, Birmingham Veterans Administration Medical Center, AL (S.S.B., S.D.P.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bindiya","family":"Patel","sequence":"additional","affiliation":[{"name":"From the Division of Cardiovascular Disease, Comprehensive Cardiovascular Center, University of Alabama at Birmingham (S.S.B., M.A.I., M.G., B.P., T.H., S.D.P.); and Medical Service, Birmingham Veterans Administration Medical Center, AL (S.S.B., S.D.P.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tariq","family":"Hamid","sequence":"additional","affiliation":[{"name":"From the Division of Cardiovascular Disease, Comprehensive Cardiovascular Center, University of Alabama at Birmingham (S.S.B., M.A.I., M.G., B.P., T.H., S.D.P.); and Medical Service, Birmingham Veterans Administration Medical Center, AL (S.S.B., S.D.P.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregg","family":"Rokosh","sequence":"additional","affiliation":[{"name":"From the Division of Cardiovascular Disease, Comprehensive Cardiovascular Center, University of Alabama at Birmingham (S.S.B., M.A.I., M.G., B.P., T.H., S.D.P.); and Medical Service, Birmingham Veterans Administration Medical Center, AL (S.S.B., 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