{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T23:29:07Z","timestamp":1791242947333,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"24","license":[{"start":{"date-parts":[[2022,11,25]],"date-time":"2022-11-25T00:00:00Z","timestamp":1669334400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2022,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Major histocompatibility complex (MHC) I is an important component of intracellular antigen presentation. However, improper expression of MHC I upon the cell surface has been associated with several autoimmune diseases. Myositis is a rare acquired autoimmune disease which targets skeletal muscle, and MHC I overexpression on the surface of muscle fibres and immune cell infiltration are clinical hallmarks. MHC I overexpression may have an important pathogenic role, mediated by the activation of the endoplasmic reticulum (ER) stress response. Given the evidence that muscle is a diverse source of cytokines, we aimed to investigate whether MHC I overexpression can modify the profile of muscle\u2010derived cytokines and what role the ER stress pathway may play. Using C2C12 myoblasts we overexpressed MHC I with a H\u20102k\n                    <jats:sup>b<\/jats:sup>\n                    vector in the presence or absence of salubrinal an ER stress pathway modifying compound. MHC I overexpression induced ER stress pathway activation and elevated cytokine gene expression. MHC I overexpression caused significant release of cytokines and chemokines, which was attenuated in the presence of salubrinal. Conditioned media from MHC I overexpressing cells induced in vitro T\u2010cell chemotaxis, atrophy of healthy myotubes and modified mitochondrial function, features which were attenuated in the presence of salubrinal. Collectively, these data suggest that MHC I overexpression can induce pro\u2010inflammatory cytokine\/chemokine release from C2C12 myoblasts, a process which appears to be mediated in\u2010part by the ER stress pathway.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.17621","type":"journal-article","created":{"date-parts":[[2022,11,25]],"date-time":"2022-11-25T03:26:48Z","timestamp":1669346808000},"page":"6032-6041","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Major histocompatibility complex I\u2010induced endoplasmic reticulum stress mediates the secretion of pro\u2010inflammatory muscle\u2010derived cytokines"],"prefix":"10.1111","volume":"26","author":[{"given":"Anastasia","family":"Thoma","sequence":"first","affiliation":[{"name":"Musculoskeletal Science &amp; Sports Medicine Research Centre, Department of Life Sciences, Faculty of Science &amp; Engineering Manchester Metropolitan University  Manchester UK"},{"name":"Sheffield Institute for Translational Neuroscience University of Sheffield  Sheffield UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kate E.","family":"Earl","sequence":"additional","affiliation":[{"name":"School of Life and Medical Sciences University of Hertfordshire  Hertfordshire UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katarzyna","family":"Goljanek\u2010Whysall","sequence":"additional","affiliation":[{"name":"Institute for Life Course and Medical Sciences University of Liverpool  Liverpool UK"},{"name":"Discipline of Physiology, School of Medicine National University of Ireland  Galway Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1501-7879","authenticated-orcid":false,"given":"Adam P.","family":"Lightfoot","sequence":"additional","affiliation":[{"name":"School of Pharmacy and Biomolecular Sciences Liverpool John Moores University  Liverpool 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