{"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":1772192767492,"version":"3.50.1"},"reference-count":37,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2004,7,1]],"date-time":"2004-07-01T00:00:00Z","timestamp":1088640000000},"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":[[2004,7,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Autoimmune response to the myelin-associated oligodendrocytic basic protein (MOBP), a CNS-specific myelin constituent, was recently suggested to play a role in the pathogenesis of multiple sclerosis (MS). The pathogenic autoimmune response to MOBP and the associated pathology in the CNS have not yet been fully investigated. In this study, we have characterized the clinical manifestations, pathology, T cell epitope-specificity, and TCRs associated with experimental autoimmune encephalomyelitis (EAE) induced in SJL\/J mice with recombinant mouse MOBP (long isoform, 170 aa). Analysis of encephalitogenic MOBP-reactive T cells for reactivity to overlapping MOBP peptides defined MOBP15\u201336 as their major immunodominant epitope. Accordingly, MOBP15\u201336 was demonstrated to be the major encephalitogenic MOBP epitope for SJL\/J mice, inducing severe\/chronic clinical EAE associated with intense perivascular and parenchymal infiltrations, widespread demyelination, axonal loss, and remarkable optic neuritis. Molecular modeling of the interaction of I-As with MOBP15\u201336, together with analysis of the MOBP15\u201336-specific T cell response to truncated peptides, suggests MOBP20\u201328 as the core sequence for I-As-restricted recognition of the encephalitogenic region MOBP15\u201336. Although highly focused in their epitope specificity, the encephalitogenic MOBP-reactive T cells displayed a widespread usage of TCR V\u03b2 genes. These results would therefore favor epitope-directed, rather than TCR-targeted, approaches to therapy of MOBP-associated pathogenic autoimmunity. Localization by molecular modeling of a potential HLA-DRB1*1501-associated MOBP epitope within the encephalitogenic MOBP15\u201336 sequence suggests the potential relevance of T cell reactivity against MOBP15\u201336 to MS. The reactivity to MOBP15\u201336 detected in MS shown here and in another study further emphasizes the potential significance of this epitope for MS.<\/jats:p>","DOI":"10.4049\/jimmunol.173.2.1426","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T19:37:22Z","timestamp":1398022642000},"page":"1426-1435","source":"Crossref","is-referenced-by-count":43,"title":["The Myelin-Associated Oligodendrocytic Basic Protein Region MOBP15\u201336 Encompasses the Immunodominant Major Encephalitogenic Epitope(s) for SJL\/J Mice and Predicted Epitope(s) for Multiple Sclerosis-Associated HLA-DRB1*1501"],"prefix":"10.1093","volume":"173","author":[{"given":"Nicole Kerlero","family":"de Rosbo","sequence":"first","affiliation":[{"name":"Immunology, Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joel F","family":"Kaye","sequence":"additional","affiliation":[{"name":"Immunology, Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Miriam","family":"Eisenstein","sequence":"additional","affiliation":[{"name":"Chemical Services, Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Itzhack","family":"Mendel","sequence":"additional","affiliation":[{"name":"Immunology, Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Romana","family":"Hoeftberger","sequence":"additional","affiliation":[{"name":"Brain Research Institute, Department of Neuroimmunology, University of Vienna , Vienna ,","place":["Austria"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hans","family":"Lassmann","sequence":"additional","affiliation":[{"name":"Brain Research Institute, Department of Neuroimmunology, University of Vienna , Vienna ,","place":["Austria"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Roni","family":"Milo","sequence":"additional","affiliation":[{"name":"Department of Neurology, Barzilai Medical Center , Ashkelon ,","place":["Israel"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Avraham","family":"Ben-Nun","sequence":"additional","affiliation":[{"name":"Immunology, Weizmann Institute of Science , Rehovot ,","place":["Israel"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2004,7,15]]},"reference":[{"key":"2026020212105186600_R1","first-page":"383","volume-title":"Immunology","year":"1998"},{"key":"2026020212105186600_R2","first-page":"189","volume-title":"J. 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