{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T19:53:55Z","timestamp":1792785235555,"version":"4.5.0"},"reference-count":53,"publisher":"National Academy of Sciences","issue":"40","license":[{"start":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:00:00Z","timestamp":1790812800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"name":"Austrian MS Society","award":["N\/A"],"award-info":[{"award-number":["N\/A"]}]},{"name":"NIH","award":["R01NS071463"],"award-info":[{"award-number":["R01NS071463"]}]},{"name":"National MS Society","award":["HC0165"],"award-info":[{"award-number":["HC0165"]}],"id":[{"id":"https:\/\/ror.org\/03019wv17","id-type":"ROR","asserted-by":"crossref"}]}],"content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2026,10,6]]},"abstract":"<jats:p>\n                    Multiple sclerosis (MS) is an autoinflammatory disease of the central nervous system (CNS). Epstein\u2013Barr virus (EBV) encodes for EBNA-1\n                    <jats:sub>381-452<\/jats:sub>\n                    , which induces autoreactive immune responses against distinct CNS derived proteins (GlialCAM\n                    <jats:sub>370-389<\/jats:sub>\n                    , CRYAB\n                    <jats:sub>2-21<\/jats:sub>\n                    , MBP\n                    <jats:sub>205-224<\/jats:sub>\n                    , ANO2\n                    <jats:sub>135-154<\/jats:sub>\n                    ). Although EBV infection is considered essential for MS development, CNS-specific autoimmune responses may also be present in putatively EBV EBNA-1-seronegative patients, warranting further investigation. We studied 548 EBV EBNA-1 seropositive and 30 EBV EBNA-1 seronegative pediatric-onset MS (POMS) patients, along with 578 matched controls. CNS specific antibodies were significantly more prevalent in EBV EBNA-1 seropositive POMS patients (92.2%) than in EBV EBNA-1 seropositive controls (56.3%,\n                    <jats:italic toggle=\"yes\">P<\/jats:italic>\n                    &lt; 0.0001). However, high CNS specific antibody levels were also found in 56.6% of EBV EBNA-1 seronegative POMS patients and 17.4% of EBV EBNA-1 seronegative controls. These findings suggest that while EBV infection amplifies CNS specific autoimmune responses, high-level CNS autoreactive autoimmune responses can also occur independently of EBV EBNA-1. We further evaluated why only some individuals with high-level CNS autoreactive antibody titers develop MS. Mechanistically, we demonstrate that autoreactive immune responses are effectively controlled by NKG2C\n                    <jats:sup>+<\/jats:sup>\n                    and NKG2D\n                    <jats:sup>+<\/jats:sup>\n                    natural killer (NK) cells. These findings indicate that CNS-specific autoimmunity and impaired NK cell regulation, rather than EBV alone, are central to MS risk.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2607529123","type":"journal-article","created":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T16:09:36Z","timestamp":1790870976000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":0,"title":["Impaired control of autoimmunity increases pediatric multiple sclerosis risk in EBNA-1-seropositives and -seronegatives"],"prefix":"10.1073","volume":"123","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3993-6538","authenticated-orcid":false,"given":"Hannes","family":"Vietzen","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05n3x4p02","id-type":"ROR","asserted-by":"publisher"}],"name":"Center for Virology, Medical University of Vienna","place":["Vienna, Austria"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5188-0157","authenticated-orcid":false,"given":"Emmanuelle L.","family":"Waubant","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/043mz5j54","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Neurology, University of California San Francisco","place":["San Francisco"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T. Charles","family":"Casper","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03r0ha626","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Pediatrics, University of Utah School of Medicine","place":["Salt Lake City"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1680-4834","authenticated-orcid":false,"given":"Leslie A.","family":"Benson","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00dvg7y05","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Neurology, Department of Neurology, Boston Children\u2019s Hospital","place":["Boston"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tanuja","family":"Chitnis","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/002pd6e78","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Pediatric Neurology, Massachusetts General Hospital, Harvard Medical 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