Autoimmunity in multiple sclerosis: role of sphingolipids, invariant NKT cells and other immune elements in control of inflammation and neurodegeneration.

Autor: Podbielska M; Department of Neurology and Neurosurgery, Medical University of South Carolina Charleston, SC, USA; Laboratory of Signal Transduction Molecules, Ludwik Hirszfeld Institute of Immunology & Experimental Therapy, Polish Academy of Sciences, Wrocław, Poland. Electronic address: maria.podbielska@iitd.pan.wroc.pl., O'Keeffe J; Department of Biopharmaceutical & Medical Science, School of Science & Computing, Galway-Mayo Institute of Technology, Galway, Ireland., Hogan EL; Department of Neurology and Neurosurgery, Medical University of South Carolina Charleston, SC, USA.
Jazyk: angličtina
Zdroj: Journal of the neurological sciences [J Neurol Sci] 2018 Feb 15; Vol. 385, pp. 198-214. Date of Electronic Publication: 2017 Dec 22.
DOI: 10.1016/j.jns.2017.12.022
Abstrakt: Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system. It is classified as being an autoimmune response in the genetically susceptible individual to a persistent but unidentified antigen(s). Both the adaptive and the innate immune systems are likely to contribute significantly to MS pathogenesis. This review summarizes current understanding of the characteristics of MS autoimmunity in the initiation and progression of the disease. In particular we find it timely to classify the autoimmune responses by focusing on the immunogenic features of myelin-derived lipids in MS including molecular mimicry; on alterations of bioactive sphingolipids mediators in MS; and on functional roles for regulatory effector cells, including innate lymphocyte populations, like the invariant NKT (iNKT) cells which bridge adaptive and innate immune systems. Recent progress in identifying the nature of sphingolipids recognition for iNKT cells in immunity and the functional consequences of the lipid-CD1d interaction opens new avenues of access to the pathogenesis of demyelination in MS as well as design of lipid antigen-specific therapeutics.
(Copyright © 2018 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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