Identification of gene expression patterns critically involved in experimental autoimmune encephalomyelitis and multiple sclerosis
| Autor: | Weissert, Robert, Herrmann, Martin M., Barth, Silvia, Greve, Bernhard, Schumann, Kathrin M., Bartels, Andrea |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
ddc:610
MYELIN OLIGODENDROCYTE GLYCOPROTEIN CELL-DERIVED FACTOR-1 CHEMOKINE RECEPTOR CXCR4 CYCLIC ADP-RIBOSE PROTEIN-KINASE T-CELLS SIGNAL-TRANSDUCTION LYMPHOID ORGANS CD38 ACTIVATION Experimental autoimmune encephalomyelitis Multiple sclerosis Central nervous system Cellular traffic T cell Adjuvant 610 Medizin |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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