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ISRN NeurologyVolume 2011 2011, Article ID 374314, 6 pages

Research Article

Department of Neurology, University of California, Irvine, CA 92868-4280, USA

Institute for Immunology, University of California, Irvine, CA 92697-4120, USA

Department of Microbiology and Molecular Genetics, University of California, Irvine, CA 92697-4025, USA

Received 9 April 2011; Accepted 30 April 2011

Academic Editors: P. Armati, M.-C. Chartier-Harlin, and J.-I. Satoh

Copyright © 2011 Ani Grigorian and Michael Demetriou. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Multiple sclerosis MS is an inflammatory demyelinating and neurodegenerative disease initiated by autoreactive T cells. 𝑀 𝑔 𝑎 𝑡 5 , a gene in the Asn N- linked protein glycosylation pathway, associates with MS severity and negatively regulates experimental autoimmune encephalomyelitis EAE and spontaneous inflammatory demyelination in mice. N-glycan branching by 𝑀 𝑔 𝑎 𝑡 5 regulates interaction of surface glycoproteins with galectins, forming a molecular lattice that differentially controls the concentration of surface glycoproteins. T-cell receptor signaling, T-cell proliferation, T H 1 differentiation, and CTLA-4 endocytosis are inhibited by 𝑀 𝑔 𝑎 𝑡 5 branching. Non-T cells also contribute to MS pathogenesis and express abundant 𝑀 𝑔 𝑎 𝑡 5 branched N-glycans. Here we explore whether 𝑀 𝑔 𝑎 𝑡 5 deficiency in myelin-reactive T cells is sufficient to promote demyelinating disease. Adoptive transfer of myelin-reactive 𝑀 𝑔 𝑎 𝑡 5 − - − T cells into 𝑀 𝑔 𝑎 𝑡 5 + - + versus 𝑀 𝑔 𝑎 𝑡 5 − - − recipients revealed more severe EAE in the latter, suggesting that 𝑀 𝑔 𝑎 𝑡 5 branching deficiency in recipient naive T cells and-or non-T cells contribute to disease pathogenesis.

Autor: Ani Grigorian and Michael Demetriou



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