ArticleEBioMedicine2020
CXCL13/CXCR5 signalling is pivotal to preserve motor neurons in amyotrophic lateral sclerosis.
Article in EBioMedicine, 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, 48 citations in OpenAlex.
- Epigenetic changes associated with the progression of prion disease in Syrian hamsters (Prion · 2026Article
- Proteomic profile of CSF obtained at the time of diagnosis determines amyotrophic lateral sclerosis progression and survival: CXCL7 levels in disease prognosis and survival.Brain pathology (Zurich, Switzerland) · 2026Article
- Dietary allergen promotes sex-specific leukocyte trafficking and alters the brain immune cell populations in subclinically sensitized mice.Brain, behavior, and immunity · 2026Article
- Decoding Neuroinflammatory Pathways: The Role of the CXCL12-CXCR4/CXCR7 Axis in ALS-Related Cognitive Impairment.Molecular neurobiology · 2026Review
- Epigenetic Changes Associated with the Progression of Prion Disease in Syrian Hamsters (Mesocricetus auratus).Research square · 2025Article
- Dynamic human gut microbiome and immune shifts during an immersive psychosocial intervention program.Brain, behavior, and immunity · 2025Observational
- Unlocking amyotrophic lateral sclerosis: the role of adiponectin in inflammation and disease progression.Frontiers in neurology · 2025Article
- Chemokine CXCL13-CXCR5 signaling in neuroinflammation and pathogenesis of chronic pain and neurological diseases.Cellular & molecular biology letters · 2024Review
- Dynamic Human Gut Microbiome and Immune Shifts During an Immersive Psychosocial Therapeutic Program.bioRxiv : the preprint server for biology · 2024Article
- The pathogenic mechanism of TAR DNA-binding protein 43 (TDP-43) in amyotrophic lateral sclerosis.Neural regeneration research · 2024Review
- Pathomechanistic Networks of Motor System Injury in Amyotrophic Lateral Sclerosis.Current neuropharmacology · 2024Review
- Dietary Polyphenols Decrease Chemokine Release by Human Primary Astrocytes Responding to Pro-Inflammatory Cytokines.Pharmaceutics · 2023Article
- CXCL13 contributes to chronic pain of a mouse model of CRPS-I via CXCR5-mediated NF-κB activation and pro-inflammatory cytokine production in spinal cord dorsal horn.Journal of neuroinflammation · 2023Article
- Loss of forebrain BIN1 attenuates hippocampal pathology and neuroinflammation in a tauopathy model.Brain : a journal of neurology · 2023Article
- Urinary biomarkers for amyotrophic lateral sclerosis: candidates, opportunities and considerations.Brain communications · 2023Review
- Neuroimmune Crosstalk Between the Peripheral and the Central Immune System in Amyotrophic Lateral Sclerosis.Frontiers in aging neuroscience · 2022Review
- Comprehensive expression analysis with cell-type-specific transcriptome in ALS-linked mutant SOD1 mice: Revisiting the active role of glial cells in disease.Frontiers in cellular neuroscience · 2022Article
- Theiler's virus-induced demyelinating disease as an infectious model of progressive multiple sclerosis.Frontiers in molecular neuroscience · 2022Review
- Contingent intramuscular boosting of P2XR7 axis improves motor function in transgenic ALS mice.Cellular and molecular life sciences : CMLS · 2021Article
- CXCL13 in Cancer and Other Diseases: Biological Functions, Clinical Significance, and Therapeutic Opportunities.Life (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCXCL13 is a B and T lymphocyte chemokine that mediates neuroinflammation through its receptor CXCR5. This chemokine is highly expressed by motoneurons (MNs) in Amyotrophic Lateral Sclerosis (ALS) SOD1G93A (mSOD1) mice during the disease, particularly in fast-progressing mice. Accordingly, in this study, we investigated the role of this chemokine in ALS.
methodsWe used in vitro and in vivo experimental paradigms derived from ALS mice and patients to investigate the expression level and distribution of CXCL13/CXCR5 axis and its role in MN death and disease progression. Moreover, we compared the levels of CXCL13 in the CSF and serum of ALS patients and controls.
findingsCXCL13 and CXCR5 are overexpressed in the spinal MNs and peripheral axons in mSOD1 mice. CXCL13 inhibition in the CNS of ALS mice resulted in the exacerbation of motor impairment (n = 4/group;Mean_Diff.=27.81) and decrease survival (n = 14_Treated:19.2 ± 1.05wks, n = 17_Controls:20.2 ± 0.6wks; 95% CI: 0.4687-1.929). This was corroborated by evidence from primary spinal cultures where the inhibition or activation of CXCL13 exacerbated or prevented the MN loss. Besides, we found that CXCL13/CXCR5 axis is overexpressed in the spinal cord MNs of ALS patients, and CXCL13 levels in the CSF discriminate ALS (n = 30) from Multiple Sclerosis (n = 16) patients with a sensitivity of 97.56%.
interpretationWe hypothesise that MNs activate CXCL13 signalling to attenuate CNS inflammation and prevent the neuromuscular denervation. The low levels of CXCL13 in the CSF of ALS patients might reflect the MN dysfunction, suggesting this chemokine as a potential clinical adjunct to discriminate ALS from other neurological diseases.
fundingVaccinex, Inc.; Regione Lombardia (TRANS-ALS).
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