Demyelination caused by the copper chelator cuprizone halts T cell mediated autoimmune neuroinflammation
Date
2009
Authors
Mana, Paula
Fordham, Susan
Staykova, Maria
Correcha, Manuel
Silva, Diego
Willenborg, D
Linares, David
Journal Title
Journal ISSN
Volume Title
Publisher
Elsevier
Abstract
Myelin reactive T cells are central in the development of the autoimmune response leading to CNS destruction in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis (EAE). Investigations on the mechanisms underlying the activation and expansion of myelin reactive T have stressed the importance of non-autoimmune conditions impinging the autoimmune repertoire potentially involved in the disease. Here, we show that CNS injury caused by the toxic cuprizone results in the generation of immunoreactivity towards several myelin components. Paradoxically, exposure to CNS injury does not increase the susceptibility to develop EAE, but render mice protected to the pathogenic autoimmune response against myelin antigens.
Description
Keywords
Keywords: chelating agent; copper; cuprizone; myelin; allergic encephalomyelitis; animal tissue; article; central nervous system; controlled study; demyelination; female; human; immune response; immunoreactivity; mouse; multiple sclerosis; nervous system inflammati Cuprizone; Demyelination; EAE; MOG; MS; Tolerance
Citation
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Source
Journal of Neuroimmunology
Type
Journal article
Book Title
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DOI
10.1016/j.jneuroim.2009.02.013
Restricted until
2037-12-31