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The Journal of Immunology, 2003, 171: 455-461.
Copyright © 2003 by The American Association of Immunologists

Selective Unresponsiveness to Conformational B Cell Epitopes of the Myelin Oligodendrocyte Glycoprotein in H-2b Mice1

Carole Bourquin*, Anna Schubart*, Stephanie Tobollik*, Ian Mather{dagger}, Sherry Ogg{dagger}, Roland Liblau{ddagger} and Christopher Linington2,§

* Department of Neuroimmunology, Max-Planck-Institute for Neurobiology, Martinsried, Germany; {dagger} Department of Animal and Avian Sciences, University of Maryland, College Park, MD 20742; {ddagger} Institut National de la Santé et de la Recherche Médicale Unité 546, Hôpital Pitié-Salpêtrière, Paris, France; and § Department of Medicine and Therapeutics, University of Aberdeen, Aberdeen, United Kingdom

Autoantibodies directed against conformation-dependent epitopes of the extracellular domain of the myelin oligodendrocyte glycoprotein (MOGIgd) play a major role in the immunopathogenesis of demyelination in experimental autoimmune encephalomyelitis. We now demonstrate that one or more genes encoded within the MHC selectively censor the ability of H-2b mice to mount this conformation-dependent autoantibody response, while leaving T and B cell responses to linear MOGIgd epitopes intact. This novel form of selective B cell unresponsiveness discriminates between pathogenic and nonpathogenic Ab responses to MOG and determines whether or not Ab-dependent effector mechanisms play an important role in the pathogenesis of MOG-induced experimental autoimmune encephalomyelitis in the mouse.




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