{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T19:31:24Z","timestamp":1791228684890,"version":"4.1.0"},"reference-count":45,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2014,12,8]],"date-time":"2014-12-08T00:00:00Z","timestamp":1417996800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"the National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["30971033"],"award-info":[{"award-number":["30971033"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2015,1]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s have been shown to be important regulators of immune homeostasis as patients with aberrant micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> expression appeared to be more susceptible to autoimmune diseases. We recently found that mi<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>\u2010146a was up\u2010regulated in activated <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> cells in response to rat acetylcholine receptor (<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>) <jats:italic>\u03b1<\/jats:italic>\u2010subunit 97\u2010116 peptide, and this up\u2010regulation was significantly attenuated by Antagomi<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>\u2010146a. Our data also demonstrated that silencing mi<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>\u2010146a with its inhibitor <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>ntagomi<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>\u2010146a effectively ameliorated clinical myasthenic symptoms in mice with ongoing experimental autoimmune myasthenia gravis. Furthermore, multiple defects were observed after mi<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>\u2010146a was knocked down in <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> cells, including decreased anti\u2010<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>97\u2010116 antibody production and class switching, reduced numbers of plasma cells, memory <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> cells and <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>\u20101 cells, and weakened activation of <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> cells. Previously, mi<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>\u2010146a has been identified as a nuclear factor\u2010\u03ba<jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>\u2010dependent gene and predicted to base pair with the tumour necrosis factor receptor\u2010associated factor 6 (<jats:styled-content style=\"fixed-case\">TRAF<\/jats:styled-content>6) and interleukin\u20101 receptor\u2010associated kinase 1 (<jats:styled-content style=\"fixed-case\">IRAK<\/jats:styled-content>1) genes to regulate the immune response. However, our study proved that mi<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>\u2010146a inhibition had no effect on the expression of <jats:styled-content style=\"fixed-case\">TRAF<\/jats:styled-content>6 and <jats:styled-content style=\"fixed-case\">IRAK<\/jats:styled-content>1 in <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> cells. This result suggests that the function of mi<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>\u2010146a in <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> cells does not involve these two target molecules. We conclude that silencing mi<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>\u2010146a exerts its therapeutic effects by influencing the <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>\u2010cell functions that contribute to the autoimmune pathogenesis of myasthenia gravis.<\/jats:p>","DOI":"10.1111\/imm.12347","type":"journal-article","created":{"date-parts":[[2014,6,24]],"date-time":"2014-06-24T21:57:38Z","timestamp":1403647058000},"page":"56-67","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":42,"title":["Silencing mi<scp>R<\/scp>\u2010146a influences <scp>B<\/scp> cells and ameliorates experimental autoimmune myasthenia gravis"],"prefix":"10.1111","volume":"144","author":[{"given":"JunMei","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Neurosurgery Xiangya Hospital Central South University Changsha Hunan 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