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Start Over Author "Bartels, Andrea" Publisher company of biologists ltd
2 results on '"Bartels, Andrea"'

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

Author

Weissert, Robert, Herrmann, Martin M., Barth, Silvia, Greve, Bernhard, Schumann, Kathrin M., and Bartels, Andrea

Subjects
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
Abstract

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.

Published
2016

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

Author

Herrmann MM, Barth S, Greve B, Schumann KM, Bartels A, and Weissert R

Subjects
ADP-ribosyl Cyclase 1 metabolism, Animals, Cell Movement drug effects, Chemokine CXCL12 metabolism, Encephalomyelitis, Autoimmune, Experimental pathology, Female, Fingolimod Hydrochloride pharmacology, Humans, Immunization, Lymph Nodes drug effects, Lymph Nodes pathology, Mice, Inbred C57BL, Multiple Sclerosis pathology, Myelin-Oligodendrocyte Glycoprotein, Peptides, RNA, Messenger genetics, RNA, Messenger metabolism, Rats, Receptors, CXCR4 genetics, Receptors, CXCR4 metabolism, Spinal Cord drug effects, Spinal Cord pathology, Encephalomyelitis, Autoimmune, Experimental genetics, Gene Expression Profiling, Gene Expression Regulation drug effects, Multiple Sclerosis genetics
Abstract

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.)

Published
2016
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