Differential expression of sema3A and sema7A in a murine model of multiple sclerosis : Implications for a therapeutic design
We characterised the expression of semaphorin (sema)3A, sema7A and their receptors in the immune and the central nervous system (CNS) at different stages of experimental autoimmune encephalomyelitis (EAE). We also studied their expression in neonatal and adult oligodendrocyte progenitor cell (OPC) a...
Veröffentlicht in: | Clinical immunology (Orlando, Fla.). - 1999. - 163(2016) vom: 21. Feb., Seite 22-33 |
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1. Verfasser: | |
Weitere Verfasser: | , , , , , , , |
Format: | Online-Aufsatz |
Sprache: | English |
Veröffentlicht: |
2016
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Zugriff auf das übergeordnete Werk: | Clinical immunology (Orlando, Fla.) |
Schlagworte: | Journal Article Research Support, Non-U.S. Gov't Experimental autoimmune encephalomyelitis Immune response Multiple sclerosis Neurodegeneration Semaphorin Antigens, CD Sema3a protein, mouse Sema7a protein, mouse mehr... |
Zusammenfassung: | We characterised the expression of semaphorin (sema)3A, sema7A and their receptors in the immune and the central nervous system (CNS) at different stages of experimental autoimmune encephalomyelitis (EAE). We also studied their expression in neonatal and adult oligodendrocyte progenitor cell (OPC) and in mature oligodendrocyte cultures. Our results show that sema3A is increased in the CNS and decreased in the immune system upon EAE induction. However, sema7A expression is increased in both the CNS and the immune system during EAE. We also detected sema3A, sema7A and their receptors in neonatal and adult OPCs and in mature oligodendrocytes. These data suggest that sema3A and sema7A are involved in the pathogenesis of EAE, in the modulation of the immune response and in the neurodegeneration that take place in the CNS. Sema7A may represent an intriguing potential therapeutic target for the treatment of both the neurodegenerative and immune-mediated disease processes in MS |
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Beschreibung: | Date Completed 28.06.2016 Date Revised 09.04.2022 published: Print-Electronic Citation Status MEDLINE |
ISSN: | 1521-7035 |
DOI: | 10.1016/j.clim.2015.12.005 |