{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T20:05:42Z","timestamp":1788984342885,"version":"build-2803163510"},"reference-count":55,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2019,1,8]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Immune cells are key regulators of the vascular inflammatory response characteristic of hypertension. In hypertensive rodents, regulatory T lymphocytes (Treg,\n              <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n              4\n              <jats:sup>+<\/jats:sup>\n              <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n              25\n              <jats:sup>+<\/jats:sup>\n              ) prevented vascular injury, cardiac damage, and endothelial dysfunction of mesenteric arteries. Whether Treg modulate the cerebrovascular damage induced by hypertension is unknown.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              C57\n              <jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\n              \/6 mice were perfused with angiotensin\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              (Ang\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              ; 1000\u00a0ng\/kg per minute) for 14\u00a0days and adoptive transfer of 3\u00d710\n              <jats:sup>5<\/jats:sup>\n              <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n              4\n              <jats:sup>+<\/jats:sup>\n              <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n              25\n              <jats:sup>+<\/jats:sup>\n              T cells was performed via 2 intravenous injections. Control mice received a sham surgery and\n              <jats:styled-content style=\"fixed-case\">PBS<\/jats:styled-content>\n              . Treg prevented Ang\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              \u2010induced neurovascular uncoupling (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05) and endothelial impairment (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05), evaluated by laser Doppler flowmetry in the somatosensory cortex. The neuroprotective effect of Treg was abolished when they were isolated from mice deficient in interleukin\u201010. Administration of interleukin\u201010 (60\u00a0ng\/d) to hypertensive mice prevented Ang\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              \u2010induced neurovascular uncoupling (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05). Treg adoptive transfer also diminished systemic inflammation induced by Ang\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05), examined with a peripheral blood cytokine array. Mice receiving Ang II + Treg exhibited reduced numbers of Iba\u20101+ cells in the brain cortex (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05) and hippocampus (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.001) compared with mice infused only with Ang II. Treg prevented the increase in cerebral superoxide radicals. Overall, these effects did not appear to be directly modulated by Treg accumulating in the brain parenchyma, because only a nonsignificant number of Treg were detected in brain. Instead, Treg penetrated peripheral tissues such as the kidney, inguinal lymph nodes, and the spleen.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Treg prevent impaired cerebrovascular responses in Ang\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              \u2010induced hypertension. The neuroprotective effects of Treg involve the modulation of inflammation in the brain and periphery.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.118.009372","type":"journal-article","created":{"date-parts":[[2018,12,21]],"date-time":"2018-12-21T10:00:25Z","timestamp":1545386425000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":30,"title":["CD4\n            <sup>+<\/sup>\n            Regulatory T Lymphocytes Prevent Impaired Cerebral Blood Flow in Angiotensin II\u2010Induced Hypertension"],"prefix":"10.1161","volume":"8","author":[{"given":"M. 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