{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,30]],"date-time":"2026-04-30T08:45:47Z","timestamp":1777538747087,"version":"3.51.4"},"reference-count":45,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2004,1,15]],"date-time":"2004-01-15T00:00:00Z","timestamp":1074124800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2004,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Previous strategies to ameliorate experimental autoimmune encephalitis (EAE) include the treatment of autoreactive T\u2004cells with altered peptide ligands, which contain amino acid substitutions at TCR contact residues. We recently showed that a variant of myelin oligodendrocyte glycoprotein (MOG)\u200435\u201355 possessing low affinity for MHC (45D) induced anergy in MOG\u200435\u201355\u2010specific T\u2004cells and reduced their encephalitogenicity upon adoptive transfer. Here we investigate the characteristics of the primary immune response to this MHC anchor\u2010substituted peptide. Overall, we observed that immunization with 45D resulted in the production of IFN\u2010\u03b3 and anti\u2010MOG\u200435\u201355 autoantibodies at levels similar to those of MOG\u200435\u201355\u2010immunized mice with active EAE. However, no symptoms of clinical or histological EAE or overt histological optic neuritis were observed in 45D\u2010immunized mice. Consistent with this finding, 45D\u2010immunized mice did not exhibit CD4<jats:sup>+<\/jats:sup> infiltrates into the CNS. Therefore, MOG\u200435\u201355\u2010specific precursors stimulated with a weak ligand (45D) mediate some EAE\u2010associated effector functions but are unable to fully initiate the inflammatory process in the central nervous system that leads to clinical manifestation of EAE.<\/jats:p>","DOI":"10.1002\/eji.200324502","type":"journal-article","created":{"date-parts":[[2004,2,4]],"date-time":"2004-02-04T12:00:38Z","timestamp":1075896038000},"page":"388-397","source":"Crossref","is-referenced-by-count":15,"title":["An MHC anchor\u2010substituted analog of myelin oligodendrocyte glycoprotein\u200435\u201355 induces IFN\u2010\u03b3 and autoantibodies in the absence of experimental autoimmune encephalomyelitis and optic neuritis"],"prefix":"10.1002","volume":"34","author":[{"given":"Mandy\u2004L.","family":"Ford","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brian\u2004D.","family":"Evavold","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2004,2,3]]},"reference":[{"key":"e_1_2_7_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81107-1"},{"key":"e_1_2_7_2_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.iy.10.040192.001101"},{"key":"e_1_2_7_3_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.20.081701.141316"},{"key":"e_1_2_7_4_2","doi-asserted-by":"publisher","DOI":"10.1007\/s001090050092"},{"key":"e_1_2_7_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830250723"},{"key":"e_1_2_7_6_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.50.3.708"},{"key":"e_1_2_7_7_2","doi-asserted-by":"publisher","DOI":"10.1007\/s004150050453"},{"key":"e_1_2_7_8_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1750-3639.1998.tb00169.x"},{"key":"e_1_2_7_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-5728(97)00203-8"},{"key":"e_1_2_7_10_2","first-page":"327","article-title":"Optic neuritis and chronic relapsing experimental allergic encephalomyelitis: relationship to clinical course and comparison with multiple sclerosis.","volume":"42","author":"Raine C. 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