{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,31]],"date-time":"2026-10-31T22:36:07Z","timestamp":1793486167658,"version":"4.5.0"},"reference-count":67,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"12","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2016,12]]},"abstract":"\n Background<\/jats:title>\n \n Excessive immune\u2010mediated inflammatory reactions play a deleterious role in postinfarction ventricular remodeling. Interleukin\u201037 (\n IL<\/jats:styled-content>\n \u201037) emerges as an inhibitor of both innate and adaptive immunity. However, the exact role of\n IL<\/jats:styled-content>\n \u201037 and\n IL<\/jats:styled-content>\n \u201037 plus troponin I (TnI)\u2013treated dendritic cells (\n DC<\/jats:styled-content>\n s) in ventricular remodeling after myocardial infarction (\n MI<\/jats:styled-content>\n ) remains elusive.\n <\/jats:p>\n <\/jats:sec>\n \n Methods and Results<\/jats:title>\n \n MI<\/jats:styled-content>\n was induced by permanent ligation of the left anterior descending artery. Our results showed that treatment with recombinant human\n IL<\/jats:styled-content>\n \u201037 significantly ameliorated ventricular remodeling after\n MI<\/jats:styled-content>\n , as demonstrated by decreased infarct size, better cardiac function, lower mortality, restricted inflammatory responses, decreased myocardial fibrosis, and inhibited cardiomyocyte apoptosis. In vitro, we examined the phenotype of\n IL<\/jats:styled-content>\n \u201037 plus TnI\u2013conditioned\n DC<\/jats:styled-content>\n s of male C57\n BL<\/jats:styled-content>\n \/6 mice and their capacity to influence the number of regulatory T cells. Our results revealed that\n IL<\/jats:styled-content>\n \u201037 plus TnI\u2013conditioned\n DC<\/jats:styled-content>\n s obtained the characteristics of tolerogenic DCs (\n tDC<\/jats:styled-content>\n s) and expanded the number of regulatory T cells when co\u2010cultured with splenic\n CD<\/jats:styled-content>\n 4\n +<\/jats:sup>\n T cells. Interestingly, we also found that adoptive transfer of these antigen\u2010loaded\n tDC<\/jats:styled-content>\n s markedly increased the number of regulatory T cells in the spleen, attenuated the infiltration of inflammatory cells in the infarct hearts, decreased myocardial fibrosis, and improved cardiac function.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Our results reveal a beneficial role of\n IL<\/jats:styled-content>\n \u201037 or\n tDC<\/jats:styled-content>\n s treated with\n IL<\/jats:styled-content>\n \u201037 plus TnI in post\u2010\n MI<\/jats:styled-content>\n remodeling that is possibly mediated by reestablishing a tolerogenic immune response, indicating that\n IL<\/jats:styled-content>\n \u201037 or adoptive transfer of\n IL<\/jats:styled-content>\n \u201037 plus TnI\u2013treated\n tDC<\/jats:styled-content>\n s may be a novel therapeutic strategy for ventricular remodeling after MI.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/jaha.116.004406","type":"journal-article","created":{"date-parts":[[2016,12,6]],"date-time":"2016-12-06T02:45:17Z","timestamp":1480992317000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":53,"title":["Interleukin\u201037 and Dendritic Cells Treated With Interleukin\u201037 Plus Troponin I Ameliorate Cardiac Remodeling After Myocardial Infarction"],"prefix":"10.1161","volume":"5","author":[{"given":"Ruirui","family":"Zhu","sequence":"first","affiliation":[{"name":"Huazhong University of Science and Technology","place":["Wuhan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haitao","family":"Sun","sequence":"additional","affiliation":[{"name":"Huazhong University of Science and Technology","place":["Wuhan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kunwu","family":"Yu","sequence":"additional","affiliation":[{"name":"Huazhong University of Science and Technology","place":["Wuhan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yucheng","family":"Zhong","sequence":"additional","affiliation":[{"name":"Huazhong University of Science and Technology","place":["Wuhan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huairui","family":"Shi","sequence":"additional","affiliation":[{"name":"Huazhong University of Science and Technology","place":["Wuhan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuzhen","family":"Wei","sequence":"additional","affiliation":[{"name":"Huazhong University of Science and Technology","place":["Wuhan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin","family":"Su","sequence":"additional","affiliation":[{"name":"Huazhong University of Science and Technology","place":["Wuhan, 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Campus","place":["Wuhan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoqi","family":"Zhao","sequence":"additional","affiliation":[{"name":"Huazhong University of Science and Technology","place":["Wuhan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuzhou","family":"Liu","sequence":"additional","affiliation":[{"name":"Huazhong University of Science and Technology","place":["Wuhan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi","family":"Mao","sequence":"additional","affiliation":[{"name":"Huazhong University of Science and Technology","place":["Wuhan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peng","family":"Cheng","sequence":"additional","affiliation":[{"name":"Huazhong University of Science and Technology","place":["Wuhan, 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