{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T16:10:14Z","timestamp":1776269414990,"version":"3.50.1"},"reference-count":34,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2012,3,2]]},"abstract":"<jats:sec>\n            <jats:title>\n              <jats:underline>Rationale:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>Atherosclerosis is a disease of large- and medium-sized arteries that is characterized by chronic vascular inflammation. While the role of Th1, Th2, and T-regulatory subsets in atherogenesis is established, the involvement of IL-17A-producing cells remains unclear.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Objective:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>To investigate the role of the IL-17A\/IL-17RA axis in atherosclerosis.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Methods and Results:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>\n              We bred apolipoprotein-E-deficient (\n              <jats:italic>\n                Apoe\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n              <\/jats:italic>\n              ) mice with IL-17A-deficient and IL-17 receptor A-deficient mice to generate\n              <jats:italic>\n                Il17a\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n                Apoe\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n              <\/jats:italic>\n              and\n              <jats:italic>\n                Il17ra\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n                Apoe\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n              <\/jats:italic>\n              mice. Western diet fed\n              <jats:italic>\n                Il17a\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n                Apoe\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n              <\/jats:italic>\n              and\n              <jats:italic>\n                Il17ra\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n                Apoe\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n              <\/jats:italic>\n              mice had smaller atherosclerotic plaques in the aortic arch and aortic roots, but showed little difference in plaque burden in the thoracoabdominal aorta in comparison with\n              <jats:italic>\n                Apoe\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n              <\/jats:italic>\n              controls. Flow cytometric analysis of\n              <jats:italic>\n                Il17a\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n                Apoe\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n              <\/jats:italic>\n              and\n              <jats:italic>\n                Il17ra\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n                Apoe\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n              <\/jats:italic>\n              aortas revealed that deficiency of IL-17A\/IL-17RA preferentially reduced aortic arch, but not thoracoabdominal aortic T cell, neutrophil, and macrophage content in comparison with\n              <jats:italic>\n                Apoe\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n              <\/jats:italic>\n              aortic segments. In contrast to ubiquitous IL-17RA expression throughout the aorta, IL-17A was preferentially expressed within the aortic arch of WD-fed\n              <jats:italic>\n                Apoe\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n              <\/jats:italic>\n              mice. Deficiency of IL-17A or IL-17RA reduced aortic arch, but not thoracoabdominal aortic TNF\u03b1 and CXCL2 expression. Aortic vascular IL-17RA supports monocyte adherence to explanted aortas in ex vivo adhesion assays. Short-term homing experiments revealed that the recruitment of adoptively transferred monocytes and neutrophils to the aortas of\n              <jats:italic>\n                Il17ra\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n                Apoe\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n              <\/jats:italic>\n              mice is impaired in comparison with\n              <jats:italic>\n                Apoe\n                <jats:sup>\u2212\/\u2212<\/jats:sup>\n              <\/jats:italic>\n              recipients.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Conclusions:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>The IL-17A\/IL-17RA axis increases aortic arch inflammation during atherogenesis through the induction of aortic chemokines, and the acceleration of neutrophil and monocyte recruitment to this site.<\/jats:p>\n          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Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, Virginia."}]},{"given":"Elena V.","family":"Galkina","sequence":"additional","affiliation":[{"name":"From the Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, 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