Time course of T-cell responses to MOG and MBP in patients with clinically isolated syndromes

CD4+ T-cell lines (TCLs) from patients with clinically isolated syndromes (CIS) were selected with purified human myelin basic protein (MBP) and recombinant human myelin oligodendrocyte glycoprotein (rhMOG), at onset of neurological symptoms and when patients developed clinically definite multiple s...

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Autor principal: Correale, J.
Otros Autores: Bassani Molinas, M.D.L.M
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Publicado: Elsevier 2003
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100 1 |a Correale, J. 
245 1 0 |a Time course of T-cell responses to MOG and MBP in patients with clinically isolated syndromes 
260 |b Elsevier  |c 2003 
270 1 0 |m Correale, J.; Department of Neurology, Raul Carrea Inst. Neurol. R., Montañeses 2325, Buenos Aires 1428, Argentina; email: jcorreale@fleni.org.ar 
506 |2 openaire  |e Política editorial 
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520 3 |a CD4+ T-cell lines (TCLs) from patients with clinically isolated syndromes (CIS) were selected with purified human myelin basic protein (MBP) and recombinant human myelin oligodendrocyte glycoprotein (rhMOG), at onset of neurological symptoms and when patients developed clinically definite multiple sclerosis (CDMS). The epitope specificity of each TCL was mapped with overlapping synthetic peptides. TCLs were assessed for their ability to secrete IFN-γ, IL-4, and IL-6. Diverse patterns of epitope recognition were observed: (a) recognition of a broad spectrum of MBP peptide epitopes with evidence of shifts over time; (b) an initial T-cell response focused to a restricted segment of the MBP molecule (83-102) that broadened over the course of disease; and (c) persistence of a focused anti-MOG T-cell response. CIS patients who failed to develop CDMS maintained a focused epitope response against two to six MBP epitopes. Most MBP peptide-specific TCLs secreted considerable amounts of IFN-γ and low amounts of IL-4 and IL-6, whereas anti rhMOGIgd peptide-specific TCLs secreted preferentially IL-4 and IL-6. These data raise important issues for the pathogenesis and treatment of multiple sclerosis (MS). © 2003 Elsevier Science B.V. All rights reserved.  |l eng 
593 |a Department of Neurology, Raul Carrea Inst. Neurol. R., Montañeses 2325, Buenos Aires 1428, Argentina 
690 1 0 |a AUTOIMMUNITY 
690 1 0 |a CLINICALLY ISOLATED SYNDROMES 
690 1 0 |a MBP 
690 1 0 |a MOG 
690 1 0 |a MULTIPLE SCLEROSIS 
690 1 0 |a ANTIBODY 
690 1 0 |a CD4 ANTIGEN 
690 1 0 |a EPITOPE 
690 1 0 |a GAMMA INTERFERON 
690 1 0 |a INTERLEUKIN 4 
690 1 0 |a INTERLEUKIN 6 
690 1 0 |a MYELIN BASIC PROTEIN 
690 1 0 |a MYELIN OLIGODENDROCYTE GLYCOPROTEIN 
690 1 0 |a ADULT 
690 1 0 |a ANTIGEN RECOGNITION 
690 1 0 |a ARTICLE 
690 1 0 |a CELL LINE 
690 1 0 |a CLINICAL ARTICLE 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a CYTOKINE RELEASE 
690 1 0 |a DISEASE COURSE 
690 1 0 |a FEMALE 
690 1 0 |a HUMAN 
690 1 0 |a MALE 
690 1 0 |a MULTIPLE SCLEROSIS 
690 1 0 |a NEUROLOGIC DISEASE 
690 1 0 |a ONSET AGE 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a T LYMPHOCYTE 
700 1 |a Bassani Molinas, M.D.L.M. 
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