{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,31]],"date-time":"2026-01-31T16:25:00Z","timestamp":1769876700526,"version":"3.49.0"},"reference-count":28,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2014,4,22]],"date-time":"2014-04-22T00:00:00Z","timestamp":1398124800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology, Japan.","award":["23592615"],"award-info":[{"award-number":["23592615"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clinical Exper Ophthalmology"],"published-print":{"date-parts":[[2015,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>To determine whether all\u2010trans retinoic acid or a synthetic retinoic acid receptor\u2010\u03b1\/\u03b2\u2010specific agonist, Am80, can reduce the degree of experimental autoimmune optic neuritis in mice with experimental autoimmune encephalomyelitis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Optic neuritis was induced in C57BL\/6 mice by immunizing them with myelin oligodendrocyte glycoprotein<jats:sub>35\u201055<\/jats:sub>. All\u2010trans retinoic acid (350\u2009\u03bcg\/mouse\/time point) or Am80 (5\u2009mg\/kg\/time point) was administered every other day from day 0 to day 20. The degree of experimental autoimmune encephalomyelitis was scored and histopathological analysis of the optic neuritis was performed on day 22 after the immunization. In vivo\u2010primed draining lymph node cells obtained from vehicle\u2010treated or all\u2010trans retinoic acid\u2010treated mice were stimulated with myelin oligodendrocyte glycoprotein<jats:sub>35\u201055<\/jats:sub>, and the culture supernatant was collected for assays of interferon\u2010\u03b3 and interleukin\u201017.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>All\u2010trans retinoic acid treatment significantly reduced the clinical score of experimental autoimmune encephalomyelitis and the severity of the optic neuritis by histopathological analysis. The production of interferon\u2010\u03b3 and interleukin\u201017 was significantly reduced in all\u2010trans retinoic acid\u2010treated mice compared with vehicle\u2010treated mice. Am80 treatment also significantly decreased the severity of the optic neuritis in mice with experimental autoimmune encephalomyelitis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These findings demonstrate that all\u2010trans retinoic acid and Am80 treatment were able to reduce the severity of optic neuritis in mice with experimental autoimmune encephalomyelitis. Activation of retinoic acid receptor\u2010\u03b1\/\u03b2 may be a molecular target for the treatment of autoimmune optic neuritis induced by Th1 or Th17\u2010dominated immune responses.<\/jats:p><\/jats:sec>","DOI":"10.1111\/ceo.12308","type":"journal-article","created":{"date-parts":[[2014,3,10]],"date-time":"2014-03-10T09:27:05Z","timestamp":1394443625000},"page":"558-567","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Retinoic acid receptor stimulation ameliorates experimental autoimmune optic neuritis"],"prefix":"10.1111","volume":"43","author":[{"given":"Hiroshi","family":"Keino","sequence":"first","affiliation":[{"name":"Department of Ophthalmology Kyorin University School of Medicine  Mitaka Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takayo","family":"Watanabe","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology Kyorin University School of Medicine  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