{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T20:05:39Z","timestamp":1787169939554,"version":"build-2736575974"},"reference-count":50,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2023,2,6]],"date-time":"2023-02-06T00:00:00Z","timestamp":1675641600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100008870","name":"National Multiple Sclerosis Society Texas Chapter","doi-asserted-by":"publisher","award":["FG\u20102108\u201038348"],"award-info":[{"award-number":["FG\u20102108\u201038348"]}],"id":[{"id":"10.13039\/100008870","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008870","name":"National Multiple Sclerosis Society Texas Chapter","doi-asserted-by":"publisher","award":["RG\u20101901\u201033219"],"award-info":[{"award-number":["RG\u20101901\u201033219"]}],"id":[{"id":"10.13039\/100008870","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunol Cell Biol"],"published-print":{"date-parts":[[2023,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    B cells play a key mechanistic role in the pathogenesis of multiple sclerosis (MS), a chronic neurological disease of the central nervous system with an autoimmune etiology. B cells contribute to disease initiation and progression by acting as professional antigen\u2010presenting cells as well as\n                    <jats:italic>via<\/jats:italic>\n                    secreting autoantibodies and proinflammatory cytokines. We have recently shown that the polyglutamine protein ataxin\u20101, which was first linked to the movement disorder spinocerebellar ataxia type 1, also acts as a master regulator of B\u2010cell functions in the context of central nervous system autoimmunity. In fact, ataxin\u20101\u2013deficient mice display an aggravated manifestation of the MS disease model experimental autoimmune encephalomyelitis along with aberrant B\u2010cell functions. Consistent with this scenario, transcriptomic analysis of\n                    <jats:italic>Atxn1<\/jats:italic>\n                    \u2010null B\u00a0cells highlighted distinct genetic signatures involved in cell activation, proliferation and antigen presentation. To further characterize the role of ataxin\u20101, we profiled the noncoding transcriptome controlled by ataxin\u20101 in the B\u2010cell compartment upon an encephalitogenic challenge. We show that two specific classes of noncoding RNAs, namely, processed pseudogenes and intergenic long noncoding RNAs, are differentially regulated along disease. Furthermore, pathway and protein network analyses on their putative protein\u2010coding gene targets found a significant enrichment in ontologies related to cell mitosis, together with molecular processes relevant to MS such as chitin metabolism. Altogether, these findings shed light on the possible contribution of noncoding RNAs to B\u2010cell biology and MS pathogenesis, and further establish the immunomodulatory role of ataxin\u20101 in autoimmune demyelination.\n                  <\/jats:p>","DOI":"10.1111\/imcb.12622","type":"journal-article","created":{"date-parts":[[2023,1,22]],"date-time":"2023-01-22T06:39:45Z","timestamp":1674369585000},"page":"358-367","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Ataxin\u20101 controls the expression of specific noncoding\n                    <scp>RNAs<\/scp>\n                    in B cells upon autoimmune demyelination"],"prefix":"10.1111","volume":"101","author":[{"given":"Qin","family":"Ma","sequence":"first","affiliation":[{"name":"Weill Institute for Neurosciences, Department of Neurology University of California  San Francisco CA 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