ArticleGlia2014
Type-I interferons suppress microglial production of the lymphoid chemokine, CXCL13.
Article in Glia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- Dietary allergen promotes sex-specific leukocyte trafficking and alters the brain immune cell populations in subclinically sensitized mice.Brain, behavior, and immunity · 2026Article
- CXCL13⁺ CD4⁺ T cells are associated with B-cell recruitment and lesion progression in cerebral cavernous malformations.Journal of neuroinflammation · 2026Article
- CRISPRi-based screen of autism spectrum disorder risk genes in microglia uncovers roles of ADNP in microglia endocytosis and synaptic pruning.Molecular psychiatry · 2025Article
- Interferon Regulatory Factors as a Potential Therapeutic Target for Neuroinflammation: A Focus on Alzheimer's Disease.International journal of molecular sciences · 2025Review
- High efficacy therapy to prevent the formation of meningeal tertiary lymphoid organs after CXCL13 index screening in early multiple sclerosis.Frontiers in neuroscience · 2025Article
- CRISPRi-based screen of Autism Spectrum Disorder risk genes in microglia uncovers roles ofbioRxiv : the preprint server for biology · 2024Article
- CXCL13: a common target for immune-mediated inflammatory diseases.Clinical and experimental medicine · 2024Review
- B cells and the stressed brain: emerging evidence of neuroimmune interactions in the context of psychosocial stress and major depression.Frontiers in cellular neuroscience · 2024Review
- Inflammation and immunomodulation in central nervous system injury - B cells as a novel therapeutic opportunity.Neurobiology of disease · 2023Review
- Multiple Sclerosis CSF Is Enriched With Follicular T Cells Displaying a Th1/Eomes Signature.Neurology(R) neuroimmunology & neuroinflammation · 2022Article
- Review
- Distinct Cellular Tropism and Immune Responses to Alphavirus Infection.Annual review of immunology · 2022Review
- Pharmacologic treatment with OKN-007 reduces alpha-motor neuron loss in spinal cord of aging mice.GeroScience · 2022Article
- Gut microbial dysbiosis after traumatic brain injury modulates the immune response and impairs neurogenesis.Acta neuropathologica communications · 2021Article
- CXCL13/CXCR5 signalling is pivotal to preserve motor neurons in amyotrophic lateral sclerosis.EBioMedicine · 2020Article
- Interaction of microglia with infiltrating immune cells in the different phases of stroke.Brain pathology (Zurich, Switzerland) · 2020Review
- Molecular Effects of FDA-Approved Multiple Sclerosis Drugs on Glial Cells and Neurons of the Central Nervous System.International journal of molecular sciences · 2020Review
- Maternal Type-I interferon signaling adversely affects the microglia and the behavior of the offspring accompanied by increased sensitivity to stress.Molecular psychiatry · 2020Article
- Impaired Innate Immunity Mechanisms in the Brain of Alzheimer's Disease.International journal of molecular sciences · 2020Article
- Role of CXCL13 in the formation of the meningeal tertiary lymphoid organ in multiple sclerosis.F1000Research · 2018Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Lymphoid chemokines are crucial for the development and maintenance of lymphoid organs, but their ectopic expression in non-lymphoid tissues is implicated in both local response to infection and chronic organ-specific autoimmunity. Production of one such chemokine, C-X-C motif ligand 13 (CXCL13), within the central nervous system (CNS) has been linked to the pathogenesis of multiple sclerosis (MS), although little is known about factors controlling its expression in different neural cell types and across a range of disease states. We provoked acute neuroinflammation in experimental animals without causing any associated demyelination using neuroadapted Sindbis virus (NSV) to better understand the sources and regulators of this chemokine in the CNS. We found that mice genetically deficient in the transcription factor, interferon (IFN) regulatory factor-7 (IRF7), made significantly higher CXCL13 protein levels in the CNS compared with wild-type (WT) controls. Microglia proved to be the main producer of CXCL13 in the brain during infection of both WT and IRF7(-/-) mice, and primary microglia cultured in vitro generated CXCL13 following stimulation with either virus particles or synthetic Toll-like receptor (TLR) ligands. Microglia cultured from IRF7(-/-) mice selectively overproduced CXCL13, and manipulation of extracellular type-I IFN levels demonstrated the existence of a negative feedback loop whereby type-I IFN receptor signaling specifically suppressed microglial CXCL13 release. Since IFN-β is used to treat patients with relapsing-remitting MS and yet acts through unknown mechanisms, we speculate that suppressed lymphoid chemokine production by microglia could contribute to its therapeutic effects.
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Registered trials
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.