{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T15:09:25Z","timestamp":1787497765311,"version":"build-2736575974"},"reference-count":64,"publisher":"Wiley","issue":"16","license":[{"start":{"date-parts":[[2021,8,12]],"date-time":"2021-08-12T00:00:00Z","timestamp":1628726400000},"content-version":"vor","delay-in-days":11,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["K01 AG061271"],"award-info":[{"award-number":["K01 AG061271"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 AG060395"],"award-info":[{"award-number":["R01 AG060395"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 AG050238"],"award-info":[{"award-number":["R01 AG050238"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 AG048366"],"award-info":[{"award-number":["R01 AG048366"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2021,8]]},"abstract":"<jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Increased large artery stiffness and impaired endothelium\u2010dependent dilatation occur with advanced age.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>We sought to determine whether T cells mechanistically contribute to age\u2010related arterial dysfunction.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>We found that old mice exhibited greater proinflammatory T cell accumulation around both the aorta and mesenteric arteries.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Pharmacologic depletion or genetic deletion of T cells in old mice resulted in ameliorated large artery stiffness and greater endothelium\u2010dependent dilatation compared with mice with T cells intact.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Ageing of the arteries is characterized by increased large artery stiffness and impaired endothelium\u2010dependent dilatation. T cells contribute to hypertension in acute rodent models but whether they contribute to chronic age\u2010related arterial dysfunction is unknown. To determine whether T cells directly mediate age\u2010related arterial dysfunction, we examined large elastic artery and resistance artery function in young (4\u20136\u00a0months) and old (22\u201324\u00a0months) wild\u2010type mice treated with anti\u2010CD3 F(ab\u20192) fragments to deplete T cells (150\u00a0\u03bcg,\n                      <jats:sc>i.p.<\/jats:sc>\n                      every 7\u00a0days for 28\u00a0days) or isotype control fragments. Old mice exhibited greater numbers of T cells in both aorta and mesenteric vasculature when compared with young mice. Old mice treated with anti\u2010CD3 fragments exhibited depletion of T cells in blood, spleen, aorta and mesenteric vasculature. Old mice also exhibited greater numbers of aortic and mesenteric IFN\u2010\u03b3 and TNF\u2010\u03b1\u2010producing T cells when compared with young mice. Old control mice exhibited greater large artery stiffness and impaired resistance artery endothelium\u2010dependent dilatation in comparison with young mice. In old mice, large artery stiffness was ameliorated with anti\u2010CD3 treatment. Anti\u2010CD3\u2010treated old mice also exhibited greater endothelium\u2010dependent dilatation than age\u2010matched controls. We also examined arterial function in young and old Rag\u20101\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                      mice, which lack lymphocytes. Rag\u20101\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                      mice exhibited blunted increases in large artery stiffness with age compared with wild\u2010type mice. Old Rag\u20101\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                      mice also exhibited greater endothelium\u2010dependent dilatation compared with old wild\u2010type mice. Collectively, these results demonstrate that T cells play an important role in age\u2010related arterial dysfunction.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp281698","type":"journal-article","created":{"date-parts":[[2021,6,24]],"date-time":"2021-06-24T01:05:02Z","timestamp":1624496702000},"page":"3973-3991","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["T cells mediate cell non\u2010autonomous arterial ageing in mice"],"prefix":"10.1113","volume":"599","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4872-4422","authenticated-orcid":false,"given":"Daniel W.","family":"Trott","sequence":"first","affiliation":[{"name":"Department of Internal Medicine University of Utah  Salt Lake City Utah USA"},{"name":"Department of Kinesiology University of Texas at Arlington  Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel R.","family":"Machin","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine University of Utah  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tam T. T.","family":"Phuong","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine University of Utah  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"AdeLola O.","family":"Adeyemo","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine University of Utah  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samuel I.","family":"Bloom","sequence":"additional","affiliation":[{"name":"Department of Nutrition and Integrative Physiology University of Utah  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. Colton","family":"Bramwell","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine University of Utah  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric S.","family":"Sorensen","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine University of Utah  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa A.","family":"Lesniewski","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine University of Utah  Salt Lake City Utah USA"},{"name":"Department of Nutrition and Integrative Physiology University of Utah  Salt Lake City Utah USA"},{"name":"Geriatrics Research Education and Clinical Center Veteran's Affairs Medical Center  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anthony J.","family":"Donato","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine University 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