Identification of gene expression patterns crucially involved in experimental autoimmune encephalomyelitis and multiple sclerosis.

Autor:	Herrmann MM; Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, 72076 Tübingen, Germany., Barth S; Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, 72076 Tübingen, Germany., Greve B; Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, 72076 Tübingen, Germany., Schumann KM; Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, 72076 Tübingen, Germany., Bartels A; Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, 72076 Tübingen, Germany., Weissert R; Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, 72076 Tübingen, Germany Department of Neurology, University of Regensburg, 93053 Regensburg, Germany robert.weissert@ukr.de.
Jazyk:	angličtina
Zdroj:	Disease models & mechanisms [Dis Model Mech] 2016 Oct 01; Vol. 9 (10), pp. 1211-1220. Date of Electronic Publication: 2016 Aug 12.
DOI:	10.1242/dmm.025536
Abstrakt:	After encounter with a central nervous system (CNS)-derived autoantigen, lymphocytes leave the lymph nodes and enter the CNS. This event leads only rarely to subsequent tissue damage. Genes relevant to CNS pathology after cell infiltration are largely undefined. Myelin-oligodendrocyte-glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis (MS), a chronic autoimmune disease of the CNS that results in disability. To assess genes that are involved in encephalitogenicity and subsequent tissue damage mediated by CNS-infiltrating cells, we performed a DNA microarray analysis from cells derived from lymph nodes and eluted from CNS in LEW.1AV1 (RT1 av1 ) rats immunized with MOG 91-108. The data was compared to immunizations with adjuvant alone or naive rats and to immunizations with the immunogenic but not encephalitogenic MOG 73-90 peptide. Here, we show involvement of Cd38, Cxcr4 and Akt and confirm these findings by the use of Cd38-knockout (B6.129P2-Cd38 tm1Lnd /J) mice, S1P-receptor modulation during EAE and quantitative expression analysis in individuals with MS. The hereby-defined underlying pathways indicate cellular activation and migration pathways mediated by G-protein-coupled receptors as crucial events in CNS tissue damage. These pathways can be further explored for novel therapeutic interventions. Competing Interests: The authors declare no competing or financial interests. (© 2016. Published by The Company of Biologists Ltd.)
Databáze:	MEDLINE
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