{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T08:07:32Z","timestamp":1790755652025,"version":"4.1.0"},"reference-count":24,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2017,4,3]],"date-time":"2017-04-03T00:00:00Z","timestamp":1491177600000},"content-version":"vor","delay-in-days":2,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["24591269"],"award-info":[{"award-number":["24591269"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2017,4]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Sporadic inclusion body myositis (sIBM), an intractable progressive muscle disease, frequently occurs in older persons. sIBM pathogenesis may involve protein degradation dysfunction and immune abnormalities. Autoantibodies recognizing cytosolic 5\u2032\u2010nucleotidase 1A (cN1A) were found in plasma and serum from sIBM patients. However, whether anti\u2010cN1A autoantibodies play a pathogenic role in sIBM is controversial. This study investigated the pathogenic properties of anti\u2010cN1A autoantibodies in sIBM pathogenesis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We developed a cell\u2010based assay to detect anti\u2010cN1A autoantibodies, which we found in serum from patients with neuromuscular diseases including sIBM. We also investigated the clinicopathological differences between sIBM patients with and without the autoantibodies. We used passive in vitro and in vivo immunization models to evaluate the pathogenic role of the autoantibodies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Of 67 patients with sIBM, 24 (35.8%) possessed anti\u2010cN1A autoantibodies as determined via our cell\u2010based assay. In the anti\u2010cN1A\u2013positive group, the percentage of patients with hepatitis C virus antibodies was significantly lower and the mean area of type 2 myofibers was significantly smaller compared with the autoantibody\u2010negative group. In the in vitro passive immunization model, p62\/SQSTM1 significantly increased in anti\u2010cN1A\u2013positive sIBM immunoglobulin G (IgG)\u2010supplemented cells. In the in vivo passive immunization model, anti\u2010cN1A\u2013positive sIBM IgG\u2010injected mice demonstrated p62\/SQSTM1\u2010positive sarcoplasmic aggregates in myofibers, associated with macrophage infiltration.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>Our cell\u2010based assay is useful for anti\u2010cN1A autoantibodies detection. Patients with anti\u2010cN1A autoantibodies demonstrated unique clinicopathological features. In vitro and in vivo passive immunization model results suggest that anti\u2010cN1A autoantibodies may affect protein degradation in myofibers. Ann Neurol 2017;81:512\u2013525<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ana.24919","type":"journal-article","created":{"date-parts":[[2017,3,20]],"date-time":"2017-03-20T05:04:49Z","timestamp":1489986289000},"page":"512-525","source":"Crossref","is-referenced-by-count":85,"title":["Pathomechanisms of anti\u2013cytosolic 5\u2032\u2010nucleotidase 1\n                    <scp>A<\/scp>\n                    autoantibodies in sporadic inclusion body myositis"],"prefix":"10.1002","volume":"81","author":[{"given":"Nozomu","family":"Tawara","sequence":"first","affiliation":[{"name":"Department of Neurology, Graduate School of Medical Sciences Kumamoto University  Kumamoto"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Satoshi","family":"Yamashita","sequence":"additional","affiliation":[{"name":"Department of Neurology, Graduate School of Medical Sciences Kumamoto University  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