ReviewNeuron2015
Dealing with Danger in the CNS: The Response of the Immune System to Injury.
Review in Neuron, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers, 2 of them syntheses 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
187 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Therapeutic local hypothermia in the management of acute spinal cord injury: a systematic review and meta-analysis.Spinal cord · 2026Pooled it
- Preclinical evidence and mechanistic insights of ligustilide in ischemic stroke: a systematic review and meta-analysis.Frontiers in pharmacology · 2025Pooled it
- Blood C-reactive protein and white blood cells trajectories and associations with clinical parameters and complications in the acute phase after subarachnoid hemorrhage.Acta neurochirurgica · 2026Article
- Review
- Article
- Co-Delivery of Sustained Release Chondroitinase ABC-37 With Human iPSC-Derived Neural Progenitors Promotes Transplant Survival and Functional Recovery in a Rodent Model of Stroke.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Infection control in the brain and the eye.Acta ophthalmologica · 2026Review
- A Dynamic and Complex Early Inflammatory Response in Blood and Cerebrospinal Fluid of Severe Traumatic Brain Injury Patients: A Dual Platform Analysis.Inflammation · 2026Observational
- Elevated phagocytic capacity directs innate spinal cord repair.Cell reports · 2026Article
- Natural killer cells aggravate neuroinflammation through microglial type I interferon pathway activation after traumatic brain injury.Journal of neuroinflammation · 2026Article
- Progress on Omega-3 fatty acids for the comprehensive and targeted treatment of spinal cord injury.Bone research · 2026Review
- Advances in cellular and molecular mechanisms of trauma-induced organ inflammation and dysfunction.Burns & trauma · 2026Review
- Nanotechnology for ischemic stroke treatment: addressing challenges across stroke management stages.Frontiers in molecular biosciences · 2026Review
- Aqueous Humor Exosomal Membrane Proteins: Decoding Pathogenic Molecular Signatures in Retinitis Pigmentosa.Translational vision science & technology · 2025Article
- Smart hybrid nanomaterials for chronic infections: microbiome-responsive and sustainable therapeutic platforms.Journal of nanobiotechnology · 2025Review
- Mechanisms underpinning spontaneous spinal cord regeneration.Development (Cambridge, England) · 2025Review
- Immunological response and tissue loss in a rodent model of chronic traumatic brain injury treated with resolvin.Journal of inflammation (London, England) · 2025Article
- Preclinical Evaluation of Pitavastatin Nanoparticles for Preserving Cone Photoreceptors in Mouse Models of RP.Investigative ophthalmology & visual science · 2025Article
- Ifi27l2a acts as a cytokine that promotes a pro-inflammatory phenotype in microglia and enhances neuroinflammation.Research square · 2025Article
- IFP35, a novel DAMP, aggravates neuroinflammation following acute ischemic stroke via TLR4/NF-κB/NLRP3 signaling.Journal of neuroinflammation · 2025Article
127 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
4 authors.
Funding
Abstract
Fighting pathogens and maintaining tissue homeostasis are prerequisites for survival. Both of these functions are upheld by the immune system, though the latter is often overlooked in the context of the CNS. The mere presence of immune cells in the CNS was long considered a hallmark of pathology, but this view has been recently challenged by studies demonstrating that immunological signaling can confer pivotal neuroprotective effects on the injured CNS. In this review, we describe the temporal sequence of immunological events that follow CNS injury. Beginning with immediate changes at the injury site, including death of neural cells and release of damage-associated molecular patterns (DAMPs), and progressing through innate and adaptive immune responses, we describe the cascade of inflammatory mediators and the implications of their post-injury effects. We conclude by proposing a revised interpretation of immune privilege in the brain, which takes beneficial neuro-immune communications into account.
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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.