{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T14:08:26Z","timestamp":1769177306665,"version":"3.49.0"},"reference-count":45,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2017,9,22]]},"abstract":"\n Background<\/jats:title>\n \n Pathogenic immune responses are known to play an important role in abdominal aortic aneurysm (\n AAA<\/jats:styled-content>\n ) development. Ultraviolet B (\n UVB<\/jats:styled-content>\n ) irradiation has been demonstrated to have therapeutic potential not only for cutaneous diseases but also for systemic inflammatory diseases in mice by suppressing immunoinflammatory responses. We investigated the effect of\n UVB<\/jats:styled-content>\n irradiation on experimental\n AAA<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>\n \n Methods and Results<\/jats:title>\n \n We used an angiotensin\n II<\/jats:styled-content>\n \u2013induced\n AAA<\/jats:styled-content>\n model in apolipoprotein E\u2013deficient mice fed a high\u2010cholesterol diet. Mice aged 10 weeks were irradiated with 5\u00a0kJ\/m\n 2<\/jats:sup>\n UVB<\/jats:styled-content>\n once weekly for 6\u00a0weeks (\n UVB<\/jats:styled-content>\n \u2010irradiated, n=38; nonirradiated, n=42) and were euthanized for evaluation of\n AAA<\/jats:styled-content>\n formation at 16\u00a0weeks. Overall, 93% of angiotensin\n II<\/jats:styled-content>\n \u2013infused mice developed\n AAA<\/jats:styled-content>\n , with 60% mortality possibly because of aneurysm rupture.\n UVB<\/jats:styled-content>\n irradiation significantly decreased the incidence (66%) and mortality (29%) of\n AAA<\/jats:styled-content>\n (\n P<\/jats:italic>\n =0.004 and\n P<\/jats:italic>\n =0.006, respectively).\n UVB<\/jats:styled-content>\n \u2010irradiated mice had significantly smaller diameter\n AAA<\/jats:styled-content>\n (\n P<\/jats:italic>\n =0.008) and fewer inflammatory cells in the aortic aneurysm tissue than nonirradiated mice, along with systemic expansion of\n CD<\/jats:styled-content>\n 4\n +<\/jats:sup>\n Foxp3\n +<\/jats:sup>\n regulatory T cells and decreased effector\n CD<\/jats:styled-content>\n 4\n +<\/jats:sup>\n CD<\/jats:styled-content>\n 44\n high<\/jats:sup>\n CD<\/jats:styled-content>\n 62L\n low<\/jats:sup>\n T cells in para\u2010aortic lymph nodes. Genetic depletion of regulatory T cells abrogated these beneficial effects of\n UVB<\/jats:styled-content>\n treatment, demonstrating a critical role of regulatory T cells.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Our data suggest that\n UVB<\/jats:styled-content>\n \u2010dependent expansion of regulatory T cells has beneficial effects on experimental\n AAA<\/jats:styled-content>\n and may provide a novel strategy for the treatment of\n AAA<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/jaha.117.007024","type":"journal-article","created":{"date-parts":[[2017,9,1]],"date-time":"2017-09-01T01:05:14Z","timestamp":1504227914000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":20,"title":["Ultraviolet B Exposure Inhibits Angiotensin II\u2013Induced Abdominal Aortic Aneurysm Formation in Mice by Expanding CD4\n +<\/sup>\n Foxp3\n +<\/sup>\n Regulatory T Cells"],"prefix":"10.1161","volume":"6","author":[{"given":"Tomohiro","family":"Hayashi","sequence":"first","affiliation":[{"name":"Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Naoto","family":"Sasaki","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan"},{"name":"Department of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomoya","family":"Yamashita","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, 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Indonesia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Keiko","family":"Yodoi","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takuya","family":"Matsumoto","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kazuyuki","family":"Kasahara","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Naofumi","family":"Yoshida","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine, 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