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Siponimod Modulates the Reaction of Microglial Cells to Pro-Inflammatory Stimulation
J. Gruchot, F. Lein, I. Lewen, L. Reiche, V. Weyers, P. Petzsch, P. Göttle, K. Köhrer, HP. Hartung, P. Küry, D. Kremer
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články
NLK
Free Medical Journals
od 2000
Freely Accessible Science Journals
od 2000
PubMed Central
od 2007
Europe PubMed Central
od 2007
ProQuest Central
od 2000-03-01
Open Access Digital Library
od 2000-01-01
Open Access Digital Library
od 2007-01-01
Health & Medicine (ProQuest)
od 2000-03-01
ROAD: Directory of Open Access Scholarly Resources
od 2000
PubMed
36362063
DOI
10.3390/ijms232113278
Knihovny.cz E-zdroje
- MeSH
- azetidiny * farmakologie metabolismus MeSH
- benzylové sloučeniny farmakologie MeSH
- lidé MeSH
- mikroglie metabolismus MeSH
- roztroušená skleróza * metabolismus MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
Siponimod (Mayzent®), a sphingosine 1-phosphate receptor (S1PR) modulator which prevents lymphocyte egress from lymphoid tissues, is approved for the treatment of relapsing-remitting and active secondary progressive multiple sclerosis. It can cross the blood-brain barrier (BBB) and selectively binds to S1PR1 and S1PR5 expressed by several cell populations of the central nervous system (CNS) including microglia. In multiple sclerosis, microglia are a key CNS cell population moving back and forth in a continuum of beneficial and deleterious states. On the one hand, they can contribute to neurorepair by clearing myelin debris, which is a prerequisite for remyelination and neuroprotection. On the other hand, they also participate in autoimmune inflammation and axonal degeneration by producing pro-inflammatory cytokines and molecules. In this study, we demonstrate that siponimod can modulate the microglial reaction to lipopolysaccharide-induced pro-inflammatory activation.
Brain and Mind Center University of Sydney Sydney NSW 2050 Australia
Department of Neurology Palacky University Olomouc 77146 Olomouc Czech Republic
Citace poskytuje Crossref.org
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