ArticleNeurology2014
Dysregulation of the IL-23/IL-17 axis and myeloid factors in secondary progressive MS.
Article in Neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Cerebrospinal Fluid and Blood Cytokines as Biomarkers for Multiple Sclerosis: A Systematic Review and Meta-Analysis of 226 Studies With 13,526 Multiple Sclerosis Patients.Frontiers in neuroscience · 2019Pooled it
- Follicle on the Roof: Tertiary Lymphoid Structures in Central Nervous System Autoimmunity.Immunological reviews · 2025Review
- Aging-dependent change in Th17 and cytokine response in multiple sclerosis.Journal of neuroinflammation · 2025Article
- SiglecF Expressing Neutrophils Exacerbate Th17-Mediated Autoimmune Neuroinflammation.Immune network · 2025Article
- Novel serum biomarker associations with 7 Tesla MRI-defined cortical lesions, leptomeningeal enhancement, and deep gray matter volume in early multiple sclerosis.Scientific reports · 2025Article
- CCL11 (Eotaxin) Promotes the Advancement of Aging-Related Cardiovascular Diseases.Reviews in cardiovascular medicine · 2025Review
- Biological aging in multiple sclerosis.Multiple sclerosis (Houndmills, Basingstoke, England) · 2023Review
- New Enhancing MRI Lesions Associate with IL-17, Neutrophil Degranulation and Integrin Microparticles: Multi-Omics Combined with Frequent MRI in Multiple Sclerosis.Biomedicines · 2023Article
- Article
- Emerging role of extracellular vesicles in multiple sclerosis: From cellular surrogates to pathogenic mediators and beyond.Journal of neuroimmunology · 2023Review
- Review
- Role of Cytokines, Chemokines and IFN-γBiomedicines · 2022Article
- Biological aging of CNS-resident cells alters the clinical course and immunopathology of autoimmune demyelinating disease.JCI insight · 2022Article
- A new and spontaneous animal model for ankylosing spondylitis is found in cynomolgus monkeys.Arthritis research & therapy · 2022Article
- Chronic traumatic encephalopathy: Diagnostic updates and advances.AIMS neuroscience · 2022Review
- Brain Antigens Stimulate Proliferation of T Lymphocytes With a Pathogenic Phenotype in Multiple Sclerosis Patients.Frontiers in immunology · 2022Article
- Article
- Pathogenic T cell cytokines in multiple sclerosis.The Journal of experimental medicine · 2020Review
- Gut microbiota-dependent CCR9+CD4+ T cells are altered in secondary progressive multiple sclerosis.Brain : a journal of neurology · 2019Article
- The Diversity of Encephalitogenic CD4+ T Cells in Multiple Sclerosis and Its Animal Models.Journal of clinical medicine · 2019Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
objectiveIn the current exploratory study, we longitudinally measured immune parameters in the blood of individuals with relapsing-remitting multiple sclerosis (RRMS) and secondary progressive multiple sclerosis (SPMS), and investigated their relationship to disease duration and clinical and radiologic measures of CNS injury.
methodsPeripheral blood mononuclear cells (PBMCs) and plasma were obtained from subjects with RRMS, SPMS, and from healthy controls on a monthly basis over the course of 1 year. MRI and Expanded Disability Status Scale evaluations were performed serially. PBMCs were analyzed by enzyme-linked immunosorbent spot assay to enumerate myelin basic protein-specific interleukin (IL)-17- and interferon (IFN)-γ-producing cells. Plasma concentrations of proinflammatory factors were measured using customized Luminex panels.
resultsFrequencies of myelin basic protein-specific IL-17- and IFN-γ-producing PBMCs were higher in individuals with RRMS and SPMS compared to healthy controls. Patients with SPMS expressed elevated levels of IL-17-inducible chemokines that activate and recruit myeloid cells. In the cohort of patients with SPMS without inflammatory activity, upregulation of myeloid-related factors correlated directly with MRI T2 lesion burden and inversely with brain parenchymal tissue volume.
conclusionsThe results of this exploratory study raise the possibility that Th17 responses and IL-17-inducible myeloid factors are elevated during SPMS compared with RRMS, and correlate with lesion burden. Our data endorse further investigation of Th17- and myeloid-related factors as candidate therapeutic targets in SPMS.
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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.