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CSF1R Stimulation Promotes Increased Neuroprotection by CD11c+ Microglia in EAE
Agnieszka Wlodarczyk1,2, Anouk Benmamar-Badel1,2, Oriane Cédile1
1Department of Neurobiology Research, Institute for Molecular Medicine, University of Southern Denmark, Odense, Denmark.
Frontiers in Cellular Neuroscience
|January 29, 2019
Summary
Stimulating Colony Stimulating Factor-1 receptor (CSF1R) expands CD11c+ microglia, reducing central nervous system inflammation and demyelination. This suggests a new therapeutic target for neuroinflammatory diseases like multiple sclerosis.
Area of Science:
- Neuroimmunology
- Cellular Biology
Background:
- Microglia, the central nervous system's immune cells, are vital for neurodevelopment and myelination.
- A specific subset, CD11c+ microglia, crucial for myelination, expands during neuroinflammation but its triggers are unknown.
- These CD11c+ microglia are implicated in protective roles in central nervous system (CNS) diseases.
Purpose of the Study:
- To identify the molecular triggers for CD11c+ microglia expansion.
- To investigate the therapeutic potential of modulating microglial populations in neuroinflammatory conditions.
Main Methods:
- Stimulation of Colony Stimulating Factor-1 receptor (CSF1R) using its ligands, CSF1 and IL-34.
- Induction of CD11c+ microglia expansion and assessment of experimental autoimmune encephalomyelitis (EAE) symptoms.
- Investigating the role of chemokine CCL2 and its receptor CCR2 in microglial expansion.
Main Results:
- CSF1R stimulation by CSF1 or IL-34 induced CD11c+ microglia expansion.
- This expansion ameliorated EAE symptoms and reduced demyelination.
- CCL2 induction by CSF1R ligands and experimental CCL2 overexpression led to CD11c+ microglia increase, suggesting a positive feedback loop involving CSF1R and CCL2.
Conclusions:
- CSF1R signaling is a key regulator of CD11c+ microglia expansion.
- Modulating CSF1R offers a potential therapeutic strategy for neuroinflammatory diseases.
- A positive feedback loop between CSF1R and CCL2 influences microglial responses in the CNS.
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