ArticleJournal of neuroinflammation2016
Expression of IL-1β in rhesus EAE and MS lesions is mainly induced in the CNS itself.
Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Role of Inflammasomes in Neuroimmune and Neurodegenerative Diseases: A Systematic Review.Mediators of inflammation · 2018Pooled it
- Phenotypic Changes in a Monocyte Cluster with High Interleukin-1 Beta Expression during Long-Term Anti-CD20 Therapy.Annals of neurology · 2025Article
- Microglia aggregates define distinct immune and neurodegenerative niches in Alzheimer's disease hippocampus.Acta neuropathologica · 2025Article
- Role of innate immune cells in multiple sclerosis.Frontiers in immunology · 2025Review
- Selected Interleukins Relevant to Multiple Sclerosis: New Directions, Potential Targets and Therapeutic Perspectives.International journal of molecular sciences · 2024Review
- PPARγ activation ameliorates cognitive impairment and chronic microglial activation in the aftermath of r-mTBI.Journal of neuroinflammation · 2024Article
- Profiling of microglia nodules in multiple sclerosis reveals propensity for lesion formation.Nature communications · 2024Article
- Biology of neurofibrosis with focus on multiple sclerosis.Frontiers in immunology · 2024Review
- Pyroptosis the Emerging Link Between Gut Microbiota and Multiple Sclerosis.Drug design, development and therapy · 2024Review
- Emodin attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis.Neural regeneration research · 2023Article
- Characterizing microglial gene expression in a model of secondary progressive multiple sclerosis.Glia · 2023Article
- Cause or consequence? The role of IL-1 family cytokines and receptors in neuroinflammatory and neurodegenerative diseases.Frontiers in immunology · 2023Article
- DNA methylation changes in glial cells of the normal-appearing white matter in Multiple Sclerosis patients.Epigenetics · 2022Article
- The nervous system during COVID-19: Caught in the crossfire.Immunological reviews · 2022Review
- Transforming growth factor-β1 protects against LPC-induced cognitive deficit by attenuating pyroptosis of microglia via NF-κB/ERK1/2 pathways.Journal of neuroinflammation · 2022Article
- Caffeine Inhibits Activation of the NLRP3 Inflammasome via Autophagy to Attenuate Microglia-Mediated Neuroinflammation in Experimental Autoimmune Encephalomyelitis.Journal of molecular neuroscience : MN · 2022Article
- Microglia Pyroptosis: A Candidate Target for Neurological Diseases Treatment.Frontiers in neuroscience · 2022Review
- The Interleukin-1 (IL-1) Superfamily Cytokines and Their Single Nucleotide Polymorphisms (SNPs).Journal of immunology research · 2022Review
- Mechanistic underpinning of an inside-out concept for autoimmunity in multiple sclerosis.Annals of clinical and translational neurology · 2021Review
- Toll-like receptor 2 and 4 antagonism for the treatment of experimental autoimmune encephalomyelitis (EAE)-related pain.Brain, behavior, and immunity · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInterleukin (IL)-1β is a pro-inflammatory cytokine that plays a role in the pathogenesis of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), the animal model for MS. Yet, detailed studies on IL-1β expression in different stages of MS lesion development and a comparison of IL-1β expression in MS and EAE are lacking.
methodsHere, we performed an extensive characterization of IL-1β expression in brain tissue of MS patients, which included different MS lesion types, and in brain tissue of rhesus macaques with EAE.
resultsIn rhesus EAE brain tissue, we observed prominent IL-1β staining in MHC class II(+) cells within perivascular infiltrates and at the edges of large demyelinating lesions. Surprisingly, staining was localized to resident microglia or differentiated macrophages rather than to infiltrating monocytes, suggesting that IL-1β expression is induced within the central nervous system (CNS). By contrast, IL-1β staining in MS brain tissue was much less pronounced. Staining was found in the parenchyma of active and chronic active MS lesions and in nodules of MHC class II(+) microglia in otherwise normal appearing white matter. IL-1β expression was detected in a minority of the nodules only, which could not be distinguished by the expression of pro- and anti-inflammatory markers. These nodules were exclusively found in MS, and it remains to be determined whether IL-1β(+) nodules are destined to progress into active lesions or whether they merely reflect a transient response to cellular stress.
conclusionsAlthough the exact localization and relative intensity of IL-1β expression in EAE and MS is different, the staining pattern in both neuroinflammatory disorders is most consistent with the idea that the expression of IL-1β during lesion development is induced in the tissue rather than in the periphery.
Indexed as
Identifiers
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.