{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T09:48:18Z","timestamp":1792144098351,"version":"4.4.0"},"reference-count":62,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"20","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Adv."],"published-print":{"date-parts":[[2023,5,19]]},"abstract":"<jats:p>\n                    Multiple sclerosis (MS) is an inflammatory disease of the central nervous system, for which Epstein-Barr virus (EBV) infection is a likely prerequisite. Due to the homology between Epstein-Barr nuclear antigen 1 (EBNA1) and alpha-crystallin B (CRYAB), we examined antibody reactivity to EBNA1 and CRYAB peptide libraries in 713 persons with MS (pwMS) and 722 matched controls (Con). Antibody response to CRYAB amino acids 7 to 16 was associated with MS (OR = 2.0), and combination of high EBNA1 responses with CRYAB positivity markedly increased disease risk (OR = 9.0). Blocking experiments revealed antibody cross-reactivity between the homologous EBNA1 and CRYAB epitopes. Evidence for T cell cross-reactivity was obtained in mice between EBNA1 and CRYAB, and increased CRYAB and EBNA1 CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cell responses were detected in natalizumab-treated pwMS. This study provides evidence for antibody cross-reactivity between EBNA1 and CRYAB and points to a similar cross-reactivity in T cells, further demonstrating the role of EBV adaptive immune responses in MS development.\n                  <\/jats:p>","DOI":"10.1126\/sciadv.adg3032","type":"journal-article","created":{"date-parts":[[2023,5,17]],"date-time":"2023-05-17T13:57:16Z","timestamp":1684331836000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":156,"title":["Cross-reactive EBNA1 immunity targets alpha-crystallin B and is associated with multiple sclerosis"],"prefix":"10.1126","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2011-1344","authenticated-orcid":true,"given":"Olivia G.","family":"Thomas","sequence":"first","affiliation":[{"name":"Therapeutic Immune Design, Center for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institute, 171 76 Stockholm, 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Switzerland."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4561-2823","authenticated-orcid":true,"given":"Andr\u00e9 Ortlieb","family":"Guerreiro-Cacais","sequence":"additional","affiliation":[{"name":"Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institute, 171 76 Stockholm, Sweden."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4882-7624","authenticated-orcid":true,"given":"Hans","family":"Gr\u00f6nlund","sequence":"additional","affiliation":[{"name":"Therapeutic Immune Design, Center for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institute, 171 76 Stockholm, Sweden."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2938-1877","authenticated-orcid":true,"given":"Tomas","family":"Olsson","sequence":"additional","affiliation":[{"name":"Neuroimmunology Unit, 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