{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T11:46:07Z","timestamp":1772192767505,"version":"3.50.1"},"reference-count":48,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2006,11,1]],"date-time":"2006-11-01T00:00:00Z","timestamp":1162339200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2006,11,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The encephalitogenic potential of oligodendrocyte-specific protein (OSP) in mice, its specific localization in the intralamellar tight junctions in CNS myelin, and the detection of autoreactivity against OSP in multiple sclerosis (MS) strongly suggest the relevance of autoreactivity against OSP in the pathogenesis of MS. In this study, we have characterized the autoimmune T and B cells that are associated with clinicopathological manifestations of OSP-induced MS-like disease in mice by using recombinant soluble mouse OSP (smOSP) and synthetic overlapping peptides spanning smOSP. SJL\/J mice immunized with smOSP developed chronic relapsing clinical experimental autoimmune encephalomyelitis accompanied with intense perivascular and parenchymal inflammatory infiltrates, widespread demyelination, axonal loss, and remarkable optic neuritis. The smOSP-primed lymph node cells reacted predominantly against OSP55\u201380 and to a lesser extent also to OSP22\u201346 and OSP179\u2013207. Unexpectedly, in vitro selection with smOSP resulted in pathogenic smOSP-specific CD4+ T cells that reacted equally well against OSP55\u201380, OSP22\u201346, OSP45\u201366, and OSP179\u2013207. Fine analysis of the anti-OSP autoimmunity revealed that the disease is primarily associated with CD4+ T cells directed against the major (OSP55\u201380) and the minor (OSP179\u2013207) encephalitogenic regions that were further delineated, both in vitro and in vivo, to OSP55\u201366 and OSP194\u2013207, respectively. In contrast, the OSP-induced Abs were predominantly directed against OSP22\u201346; these Abs were mostly of IgG1 isotype, but high levels of IgG2a and IgG2b and significant levels of IgE were also observed. The reactivity of pathogenic T cells to two encephalitogenic regions, OSP55\u201380 and OSP179\u2013207, and their diverse TCRV\u03b2 gene repertoire may impose difficulties for epitope-directed or TCR-targeting approaches to immune-specific modulation of OSP-related pathogenesis.<\/jats:p>","DOI":"10.4049\/jimmunol.177.10.7364","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T19:39:04Z","timestamp":1397849944000},"page":"7364-7376","source":"Crossref","is-referenced-by-count":27,"title":["Epitope Specificity of Autoreactive T and B Cells Associated with Experimental Autoimmune Encephalomyelitis and Optic Neuritis Induced by Oligodendrocyte-Specific Protein in SJL\/J Mice"],"prefix":"10.1093","volume":"177","author":[{"given":"Nathali","family":"Kaushansky","sequence":"first","affiliation":[{"name":"Department of Immunology, The Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ming-Chao","family":"Zhong","sequence":"additional","affiliation":[{"name":"Department of Immunology, The Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nicole","family":"Kerlero de Rosbo","sequence":"additional","affiliation":[{"name":"Department of Immunology, The Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Romana","family":"Hoeftberger","sequence":"additional","affiliation":[{"name":"Clinical Institute of Neurology, Medical University of Vienna , Vienna ,","place":["Austria"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hans","family":"Lassmann","sequence":"additional","affiliation":[{"name":"Center for Brain Research, Department of Neuroimmunology, Medical University of Vienna , Vienna ,","place":["Austria"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Avraham","family":"Ben-Nun","sequence":"additional","affiliation":[{"name":"Department of Immunology, The Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2006,11,15]]},"reference":[{"key":"2026020214061407800_R1","first-page":"287","volume-title":"J. 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