{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T19:00:34Z","timestamp":1784746834186,"version":"3.55.0"},"reference-count":51,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>\n                      Persistent inflammation is linked to poor outcomes in patients with a history of myocardial infarction. The inflammatory state has been associated with activation of neutrophils as well as with regulatory T-cell (T\n                      <jats:sub>reg<\/jats:sub>\n                      ) deficiency. The role of T\n                      <jats:sub>regs<\/jats:sub>\n                      in the regulation of neutrophil survival has been postulated recently. Here, we investigated neutrophil apoptosis along with the potential impact of T\n                      <jats:sub>regs<\/jats:sub>\n                      on neutrophil apoptosis in patients with postmyocardial infarction chronic coronary syndrome, compared with healthy controls.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      Twenty patients and 19 controls were included. Neutrophil apoptosis was assessed after 5-hour culture with or without IL (interleukin)-10, TNF (tumor necrosis factor), or lipopolysaccharide. Neutrophil phenotype was evaluated through flow cytometry analysis of surface receptors (CD66b [cluster of differentiation] and CXCR4 [C-X-C chemokine receptor type 4]) and ex vivo release of cytokines and proteins. The ability of T\n                      <jats:sub>regs<\/jats:sub>\n                      to induce neutrophil apoptosis was examined in autologous neutrophil-T\n                      <jats:sub>reg<\/jats:sub>\n                      cocultures.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      Spontaneous neutrophil apoptosis was significantly delayed in patients compared with controls (10.3% versus 19.2%,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.025). Also, neutrophils from patients overexpressed CD66b and CXCR4 and were more prone to release proinflammatory mediators. Notably, T\n                      <jats:sub>regs<\/jats:sub>\n                      induced neutrophil apoptosis in healthy subjects, but not in patients, indicating a loss of T\n                      <jats:sub>reg<\/jats:sub>\n                      -mediated regulation in the latter. There was no evidence that IL-10 had any influence on neutrophil apoptosis. However, cell-to-cell contact was found essential for T\n                      <jats:sub>reg<\/jats:sub>\n                      -induced neutrophil apoptosis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>\n                      Patients with postmyocardial infarction chronic coronary syndrome display delayed neutrophil apoptosis and a proinflammatory neutrophil phenotype that is resistant to T\n                      <jats:sub>reg<\/jats:sub>\n                      -mediated apoptosis. Neutrophil dysfunction may contribute to persistent inflammation in patients with postmyocardial infarction chronic coronary syndrome, and as such constitutes a novel therapeutic target.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/atvbaha.126.324652","type":"journal-article","created":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T09:00:38Z","timestamp":1782378038000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Neutrophils Exhibit Delayed Spontaneous Apoptosis and Resistance to Regulatory T-Cell\u2013Induced Apoptosis in Patients With Chronic Coronary Syndrome\u2014Brief Report"],"prefix":"10.1161","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-0230-0369","authenticated-orcid":true,"given":"Maike","family":"Schneider","sequence":"first","affiliation":[{"name":"Department of Health, Medicine, and Caring Sciences, Link\u00f6ping University, Sweden (M.S., C.S., R.W.S.C., L.J.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4770-8594","authenticated-orcid":true,"given":"Camilla","family":"Skoglund","sequence":"additional","affiliation":[{"name":"Department of Health, Medicine, and Caring Sciences, Link\u00f6ping University, Sweden (M.S., C.S., R.W.S.C., L.J.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9959-5849","authenticated-orcid":true,"given":"Rosanna W.S.","family":"Chung","sequence":"additional","affiliation":[{"name":"Department of Health, Medicine, and Caring Sciences, Link\u00f6ping University, Sweden (M.S., C.S., R.W.S.C., L.J.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0586-6618","authenticated-orcid":true,"given":"Lena","family":"Jonasson","sequence":"additional","affiliation":[{"name":"Department of Health, Medicine, and Caring Sciences, Link\u00f6ping University, Sweden (M.S., C.S., R.W.S.C., L.J.)."},{"name":"Clinical Department of Cardiology, Region \u00d6sterg\u00f6tland, Link\u00f6ping, Sweden (L.J.)."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2019.07.061"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2025.09.012"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/ATVBAHA.114.303564"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehad649"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvz084"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1161\/JAHA.124.036701"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.3390\/jcm9051602"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2009.07.037"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.vph.2022.107098"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000163262.83456.6d"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2004.03.013"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2006.08.003"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0019340"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0001056"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1016\/s1074-7613(03)00263-2"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41420-020-0255-6"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.molimm.2007.10.013"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.24634"},{"key":"e_1_3_3_20_2","first-page":"885","article-title":"Delayed neutrophil apoptosis in very early rheumatoid arthritis patients is abrogated by methotrexate therapy.","volume":"25","author":"Weinmann P","year":"2007","unstructured":"Weinmann P, Moura RA, Caetano-Lopes JR, Pereira PA, Canh\u00e3o H, Queiroz MV, Fonseca JE., , Delayed neutrophil apoptosis in very early rheumatoid arthritis patients is abrogated by methotrexate therapy. Clin Exp Rheumatol. 2007;25:885\u2013887.","journal-title":"Clin Exp Rheumatol"},{"key":"e_1_3_3_21_2","doi-asserted-by":"publisher","DOI":"10.1097\/00024382-200005000-00003"},{"key":"e_1_3_3_22_2","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0703358"},{"key":"e_1_3_3_23_2","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehp248"},{"key":"e_1_3_3_24_2","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehl222"},{"key":"e_1_3_3_25_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2012.03.016"},{"key":"e_1_3_3_26_2","doi-asserted-by":"publisher","DOI":"10.1111\/joim.12398"},{"key":"e_1_3_3_27_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.177.10.7155"},{"key":"e_1_3_3_28_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1600954"},{"key":"e_1_3_3_29_2","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2019.00680"},{"key":"e_1_3_3_30_2","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2023.1287465"},{"key":"e_1_3_3_31_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jim.2022.113403"},{"key":"e_1_3_3_32_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.1996.271.4.L566"},{"key":"e_1_3_3_33_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1574-695X.1996.tb00084.x"},{"key":"e_1_3_3_34_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.cir.88.2.358"},{"key":"e_1_3_3_35_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2016-05-718999"},{"key":"e_1_3_3_36_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-023-41484-3"},{"key":"e_1_3_3_37_2","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0608382"},{"key":"e_1_3_3_38_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.intimp.2018.03.025"},{"key":"e_1_3_3_39_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.athoracsur.2006.10.065"},{"key":"e_1_3_3_40_2","doi-asserted-by":"publisher","DOI":"10.1016\/S2213-2600(14)70050-5"},{"key":"e_1_3_3_41_2","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2019.00159"},{"key":"e_1_3_3_42_2","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2021.626193"},{"key":"e_1_3_3_43_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.intimp.2023.109824"},{"key":"e_1_3_3_44_2","doi-asserted-by":"publisher","DOI":"10.1134\/S0022093021030017"},{"key":"e_1_3_3_45_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41590-018-0120-4"},{"key":"e_1_3_3_46_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2011.03.018"},{"key":"e_1_3_3_47_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni.3224"},{"key":"e_1_3_3_48_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V90.9.3356"},{"key":"e_1_3_3_49_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.200425561"},{"key":"e_1_3_3_50_2","doi-asserted-by":"publisher","DOI":"10.1038\/mi.2015.66"},{"key":"e_1_3_3_51_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.188.2.287"},{"key":"e_1_3_3_52_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.imbio.2012.05.029"}],"container-title":["Arteriosclerosis, Thrombosis, and Vascular Biology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ahajournals.org\/doi\/full\/10.1161\/ATVBAHA.126.324652","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T18:00:51Z","timestamp":1784743251000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ahajournals.org\/doi\/10.1161\/ATVBAHA.126.324652"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2026,8]]},"references-count":51,"journal-issue":{"issue":"8","published-print":{"date-parts":[[2026,8]]}},"alternative-id":["10.1161\/ATVBAHA.126.324652"],"URL":"https:\/\/doi.org\/10.1161\/atvbaha.126.324652","relation":{},"ISSN":["1079-5642","1524-4636"],"issn-type":[{"value":"1079-5642","type":"print"},{"value":"1524-4636","type":"electronic"}],"subject":[],"published":{"date-parts":[[2026,8]]},"assertion":[{"value":"2026-03-06","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2026-06-10","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2026-06-25","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}