ArticleFrontiers in immunology2020
Inhibition of IL-34 Unveils Tissue-Selectivity and Is Sufficient to Reduce Microglial Proliferation in a Model of Chronic Neurodegeneration.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Human IL-34 Deficiency Primes Microglia Toward Alzheimer's Disease-Associated States.medRxiv : the preprint server for health sciences · 2026Article
- IL-34 in neurological homeostasis and its multifaceted roles in central nervous system diseases.Frontiers in immunology · 2026Review
- Roles of IL-34 in neurological diseases: neuroprotection, inflammatory regulation, and myeloid plasticity.Frontiers in immunology · 2026Review
- Defined human tri-lineage brain microtissues.bioRxiv : the preprint server for biology · 2025Article
- CD4Frontiers in immunology · 2025Article
- Molecular landscape of the overlap between Alzheimer's disease and somatic insulin-related diseases.Alzheimer's research & therapy · 2024Article
- The molecular determinants of microglial developmental dynamics.Nature reviews. Neuroscience · 2024Review
- Effects of IL-34 and anti-IL-34 neutralizing mAb on alveolar bone loss in a ligature-induced model of periodontitis.Molecular oral microbiology · 2024Article
- The aging mouse CNS is protected by an autophagy-dependent microglia population promoted by IL-34.Nature communications · 2024Article
- A fast non-parametric test of association for multiple traits.Genome biology · 2023Article
- Towards using 3D cellular cultures to model the activation and diverse functions of macrophages.Biochemical Society transactions · 2023Review
- Single-cell-led drug repurposing for Alzheimer's disease.Scientific reports · 2023Article
- Enhanced M-CSF/CSF1R Signaling Closely Associates with PrPMolecular neurobiology · 2022Article
- Review
- Attack of the Clones: Microglia in Health and Disease.Frontiers in cellular neuroscience · 2022Article
- TNFAIP3 Reduction-of-Function Drives Female Infertility and CNS Inflammation.Frontiers in immunology · 2022Article
- Colony stimulating factors in the nervous system.Seminars in immunology · 2021Review
- Conditional genetic deletion of CSF1 receptor in microglia ameliorates the physiopathology of Alzheimer's disease.Alzheimer's research & therapy · 2021Article
- To Kill a Microglia: A Case for CSF1R Inhibitors.Trends in immunology · 2020Review
- Inhibition of IL-34 Unveils Tissue-Selectivity and Is Sufficient to Reduce Microglial Proliferation in a Model of Chronic Neurodegeneration.Frontiers in immunology · 2020Article
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Authors and funding
18 authors at 7 institutions in 1 country.
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Abstract
The proliferation and activation of microglia, the resident macrophages in the brain, is a hallmark of many neurodegenerative diseases such as Alzheimer's disease (AD) and prion disease. Colony stimulating factor 1 receptor (CSF1R) is critically involved in regulating microglial proliferation, and CSF1R blocking strategies have been recently used to modulate microglia in neurodegenerative diseases. However, CSF1R is broadly expressed by many cell types and the impact of its inhibition on the innate immune system is still unclear. CSF1R can be activated by two independent ligands, CSF-1 and interleukin 34 (IL-34). Recently, it has been reported that microglia development and maintenance depend on IL-34 signaling. In this study, we evaluate the inhibition of IL-34 as a novel strategy to reduce microglial proliferation in the ME7 model of prion disease. Selective inhibition of IL-34 showed no effects on peripheral macrophage populations in healthy mice, avoiding the side effects observed after CSF1R inhibition on the systemic compartment. However, we observed a reduction in microglial proliferation after IL-34 inhibition in prion-diseased mice, indicating that microglia could be more specifically targeted by reducing IL-34. Overall, our results highlight the challenges of targeting the CSF1R/IL34 axis in the systemic and central compartments, important for framing any therapeutic effort to tackle microglia/macrophage numbers during brain disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.