Four different synthetic peptides of proteolipid protein induce a distinct antibody response in MP4-induced experimental autoimmune encephalomyelitis

Four different synthetic peptides of proteolipid protein induce a distinct antibody response in MP4-induced experimental autoimmune encephalomyelitis

Copyright © 2015 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 159(2015), 1 vom: 11. Juli, Seite 93-106
1. Verfasser: Recks, Mascha S (VerfasserIn)
Weitere Verfasser: Grether, Nicolai B, van der Broeck, Franziska, Ganscher, Alla, Wagner, Nicole, Henke, Erik, Ergün, Süleyman, Schroeter, Michael, Kuerten, Stefanie
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2015
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Animal models Antibodies Autoimmunity B cells Multiple sclerosis Epitopes MP4 protein, chimeric Myelin Basic Protein mehr... Myelin Proteolipid Protein Peptide Fragments Recombinant Fusion Proteins
Beschreibung
Zusammenfassung:Copyright © 2015 Elsevier Inc. All rights reserved.
Here we studied the autoantibody specificity elicited by proteolipid protein (PLP) in MP4-induced experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis (MS). In C57BL/6 (B6) mice, antibodies were induced by immunization with one of the two extracellular and by the intracellular PLP domain. Antibodies against extracellular PLP were myelin-reactive in oligodendrocyte cultures and induced mild spinal cord demyelination upon transfer into B cell-deficient J(H)T mice. Remarkably, also antibodies against intracellular PLP showed binding to intact oligodendrocytes and were capable of inducing myelin pathology upon transfer into J(H)T mice. In MP4-immunized mice peptide-specific T(H)1/T(H)17 responses were mainly directed against the extracellular PLP domains, but also involved the intracellular epitopes. These data suggest that both extracellular and intracellular epitopes of PLP contribute to the pathogenesis of MP4-induced EAE already in the setting of intact myelin. It remains to be elucidated if this concept also applies to MS itself
Beschreibung:Date Completed 24.08.2015
Date Revised 13.06.2015
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2015.04.020