ArticleProceedings of the National Academy of Sciences of the United States of America2022
CSF-1 maintains pathogenic but not homeostatic myeloid cells in the central nervous system during autoimmune neuroinflammation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 42 citations in OpenAlex.
- Multi-dimensional decoding of the TSPO signal in animal models of neuroinflammation using fluorescence-conjugated DPA714.Journal of neuroinflammation · 2026Article
- In vivo CRISPR screen reveals regulation of macrophage states in neuroinflammation.Nature neuroscience · 2026Article
- Extracellular vesicle-derived miR-760 as a novel promising candidate biomarker differentiating stable RRMS from SPMS.Scientific reports · 2026Article
- Roles of IL-34 in neurological diseases: neuroprotection, inflammatory regulation, and myeloid plasticity.Frontiers in immunology · 2026Review
- IL-34 in neurological homeostasis and its multifaceted roles in central nervous system diseases.Frontiers in immunology · 2026Review
- Glucose metabolic reprogramming: mechanisms and therapeutic implications in neuroinflammation.Frontiers in immunology · 2026Review
- Expression of Macrophage Colony-Stimulating Factor 1 (CSF-1) by Spinal Cord Astrocytes in Mice with Experimental Autoimmune Encephalomyelitis.Bulletin of experimental biology and medicine · 2025Article
- Myelopoiesis is temporally dynamic and is regulated by lifestyle to modify multiple sclerosis.Nature communications · 2025Article
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- Myeloid cell replacement is neuroprotective in chronic experimental autoimmune encephalomyelitis.Nature neuroscience · 2024Article
- CSF1R antagonism results in increased supraspinal infiltration in EAE.Journal of neuroinflammation · 2024Article
- Single-Cell Profiling Indicates a Proinflammatory Role of Meningeal Ectopic Lymphoid Tissue in Experimental Autoimmune Encephalomyelitis.Neurology(R) neuroimmunology & neuroinflammation · 2024Article
- Exploration of the causal associations between circulating inflammatory proteins, immune cells, and neuromyelitis optica spectrum disorder: a bidirectional Mendelian randomization study and mediation analysis.Frontiers in aging neuroscience · 2024Article
- Ablation of microglia following infection of the central nervous system with a neurotropic murine coronavirus infection leads to increased demyelination and impaired remyelination.Journal of neuroimmunology · 2023Article
- Roles and regulation of microglia activity in multiple sclerosis: insights from animal models.Nature reviews. Neuroscience · 2023Review
- Augmentation of a neuroprotective myeloid state by hematopoietic cell transplantation.bioRxiv : the preprint server for biology · 2023Article
- CSF-1 and Notch signaling cooperate in macrophage instruction and tissue repair during peripheral limb ischemia.Frontiers in immunology · 2023Article
- GATA1 controls numbers of hematopoietic progenitors and their response to autoimmune neuroinflammation.Blood advances · 2022Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
The receptor for colony stimulating factor 1 (CSF-1R) is important for the survival and function of myeloid cells that mediate pathology during experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). CSF-1 and IL-34, the ligands of CSF-1R, have similar bioactivities but distinct tissue and context-dependent expression patterns, suggesting that they have different roles. This could be the case in EAE, given that CSF-1 expression is up-regulated in the CNS, while IL-34 remains constitutively expressed. We found that targeting CSF-1 with neutralizing antibody halted ongoing EAE, with efficacy superior to CSF-1R inhibitor BLZ945, whereas IL-34 neutralization had no effect, suggesting that pathogenic myeloid cells were maintained by CSF-1. Both anti–CSF-1 and BLZ945 treatment greatly reduced the number of monocyte-derived cells and microglia in the CNS. However, anti–CSF-1 selectively depleted inflammatory microglia and monocytes in inflamed CNS areas, whereas BLZ945 depleted virtually all myeloid cells, including quiescent microglia, throughout the CNS. Anti–CSF-1 treatment reduced the size of demyelinated lesions and microglial activation in the gray matter. Lastly, we found that bone marrow–derived immune cells were the major mediators of CSF-1R–dependent pathology, while microglia played a lesser role. Our findings suggest that targeting CSF-1 could be effective in ameliorating MS pathology, while preserving the homeostatic functions of myeloid cells, thereby minimizing risks associated with ablation of CSF-1R–dependent cells.
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