ArticleAnnals of neurology2015
A destructive feedback loop mediated by CXCL10 in central nervous system inflammatory disease.
Article in Annals of neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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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
18 citing papers in PubMed, 27 citations in OpenAlex.
- T cell acute lymphoblastic leukemia exploits a neural proinflammatory pathway to colonize the meninges.The Journal of clinical investigation · 2026Article
- C‑X‑C Motif Chemokine 10/C-X‑C Motif Chemokine Receptor 3 Signaling Induces Neural Senescence and Cognitive Impairments.ACS pharmacology & translational science · 2025Article
- Toward curing neurological autoimmune disorders: Biomarkers, immunological mechanisms, and therapeutic targets.Neuron · 2025Review
- Neuroimmune crosstalk in chronic neuroinflammation: microglial interactions and immune modulation.Frontiers in cellular neuroscience · 2025Review
- CXCL10 Is Associated with Increased Cerebrospinal Fluid Immune Cell Infiltration and Disease Duration in Multiple Sclerosis.Biomolecules · 2023Article
- Cytokine dynamics and targeted immunotherapies in autoimmune encephalitis.Brain communications · 2022Review
- Anti-neuron antibody syndrome: clinical features, cytokines/chemokines and predictors.Journal of neuroinflammation · 2021Article
- IFN-γ- and IL-17-producing CD8Journal for immunotherapy of cancer · 2021Article
- Neuropsychiatric Disorders Due to Limbic Encephalitis: Immunologic Aspect.International journal of molecular sciences · 2020Review
- Chronic Inflammatory Lameness Increases Cytokine Concentration in the Spinal Cord of Dairy Cows.Frontiers in veterinary science · 2020Article
- Immunological Bases of Paraneoplastic Cerebellar Degeneration and Therapeutic Implications.Frontiers in immunology · 2020Review
- Effective effectors: How T cells access and infiltrate the central nervous system.Pharmacology & therapeutics · 2019Review
- IFN-γ is a therapeutic target in paraneoplastic cerebellar degeneration.JCI insight · 2019Article
- The Role of CXCR3 in Neurological Diseases.Current neuropharmacology · 2019Review
- Advances in Biomarker-Guided Therapy for Pediatric- and Adult-Onset Neuroinflammatory Disorders: Targeting Chemokines/Cytokines.Frontiers in immunology · 2018Review
- Serum IFN-γ-induced protein 10 (IP-10) as a biomarker for severity of acute respiratory infection in healthy adults.Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2017Article
- Article
- Noninvasive profiling of serum cytokines in breast cancer patients and clinicopathological characteristics.OncoimmunologyArticle
Corrections and comments
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- Commented on byReply.2016
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
objectiveParaneoplastic neurologic disorders (PND) are autoimmune diseases associated with cancer and ectopic expression of a neuronal antigen in a peripheral tumor. Patients with PND harbor high-titer antibodies and T cells in their serum and cerebrospinal fluid (CSF) that are specific to the tumor antigen, and treatment with the immunosuppressant FK506 (tacrolimus) decreases CSF white blood cell counts. The objective of this study was to determine the effect of FK506 on CSF chemokine levels in PND patients.
methodsCSF samples before and after FK506 treatment were tested by multiplex assay for the presence of 27 cytokines. Follow-up in vitro experiments aimed to determine whether T cells secrete CXCL10 in response to cognate antigen.
resultsHere we report that PND patients harbor high levels of the chemokine CXCL10 in their CSF. CXCL10 is a cytokine that recruits CXCR3(+) cells such as activated T cells, and we found that FK506 treatment specifically decreased CSF CXCL10 from among 27 cytokines tested. In vitro, CXCL10 was only produced during antigen-specific cognate interactions between T cells and antigen-presenting cells (APCs) when interferon-γ (IFNγ) receptors were present on the T cell.
interpretationThese results support a model in which antigen-specific T cell stimulation by PND APCs triggers IFNγ, followed by CXCL10 production and further lymphocyte recruitment, suggesting that treatments targeting T cells or CXCL10 in the central nervous system (CNS) may interrupt a destructive positive feedback loop present in CNS inflammation.
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What OpenQuestion holds
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.