ArticleProceedings of the National Academy of Sciences of the United States of America2018
IL-1β enables CNS access to CCR2
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 91 citations in OpenAlex.
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- Autophagy-NLRP3 Inflammasome Crosstalk in Microglia: A Therapeutic Target for Multiple Sclerosis.Inflammation · 2026Review
- Aging, the microbiota-gut-brain axis, and late-life epilepsy: a hypothesis-driven review.Frontiers in molecular neuroscience · 2026Review
- MK2 deficiency decreases mortality in male mice during the inflammatory phase after myocardial infarction.Physiological reports · 2025Article
- CRTH2 is critical for IL-1β-producing B cells during experimental autoimmune encephalomyelitis in mice via p38 signaling.Journal of neuroinflammation · 2025Article
- Brain Endothelial Cells in Blood-Brain Barrier Regulation and Neurological Therapy.International journal of molecular sciences · 2025Review
- CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model.Nature neuroscience · 2025Article
- The interaction between central and peripheral immune systems in methamphetamine use disorder: current status and future directions.Journal of neuroinflammation · 2025Review
- Macrophage-targeted PEGylated liposomes ameliorate experimental autoimmune encephalomyelitis.Frontiers in immunology · 2025Article
- A miR-383-5p Signaling Hub Coordinates the Axon Regeneration Response to Inflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- The Immunometabolic Gene N-Acetylglucosamine Kinase Is Uniquely Involved in the Heritability of Multiple Sclerosis Severity.International journal of molecular sciences · 2024Article
- Treated and Untreated Primary Progressive Multiple Sclerosis: Walkthrough Immunological Changes of Monocytes and T Regulatory Cells.Biomedicines · 2024Article
- Unravelling monocyte functions: from the guardians of health to the regulators of disease.Discovery immunology · 2024Review
- Expression of CD40 and CD192 in Classical Monocytes in Multiple Sclerosis Patients Assessed with Transcranial Magnetic Stimulation.Biomedicines · 2023Article
- JAK inhibition ameliorated experimental autoimmune encephalomyelitis by blocking GM-CSF-driven inflammatory signature of monocytes.Acta pharmaceutica Sinica. B · 2023Article
- Roles and regulation of microglia activity in multiple sclerosis: insights from animal models.Nature reviews. Neuroscience · 2023Review
- Advancements in Macrophage-Targeted Drug Delivery for Effective Disease Management.International journal of nanomedicine · 2023Review
- The alarmin interleukin-1α triggers secondary degeneration through reactive astrocytes and endothelium after spinal cord injury.Nature communications · 2022Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Molecular interventions that limit pathogenic CNS inflammation are used to treat autoimmune conditions such as multiple sclerosis (MS). Remarkably, IL-1β-knockout mice are highly resistant to experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Here, we show that interfering with the IL-1β/IL-1R1 axis severely impairs the transmigration of myeloid cells across central nervous system (CNS) endothelial cells (ECs). Notably, we report that IL-1β expression by inflammatory CCR2
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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.