ArticleNeural regeneration research2019
Interleukin-4 affects microglial autophagic flux.
Article in Neural regeneration research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Regulatory role of the endocannabinoid system on glial cells toward cognitive function in Alzheimer's disease: A systematic review and meta-analysis of animal studies.Frontiers in pharmacology · 2023Pooled it
- Low-dose interleukin-2 in patients with mild to moderate Alzheimer's disease: a randomized clinical trial.Alzheimer's research & therapy · 2025Trial
- Transcriptomic Signatures of Microglial Phagocytosis Reveal Diagnostic Markers and Immune Landscape in Alzheimer's Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- IL-4 in Alzheimer's Disease-Mechanisms and Therapeutic Potential.Molecular neurobiology · 2026Review
- Leveraging machine learning and network biology approaches to predict brain gene expression from blood transcriptomes.GigaScience · 2026Article
- Autophagy in ocular diseases: from mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- Antibody targeting TDP-43 mitigates pathogenic pathways induced by the cerebrospinal fluid of ALS.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Brain interleukins and Alzheimer's disease.Metabolic brain disease · 2025Review
- Stem Cell Interventions in the Treatment of Alzheimer's Disease.Current stem cell research & therapy · 2025Review
- Virus-induced brain pathology and the neuroinflammation-inflammation continuum: the neurochemists view.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- "Let's talk about sex, inflammaging, and cognition, baby": A meta-analysis and meta-regression of 106 case-control studies on mild cognitive impairment and Alzheimer's disease.Brain, behavior, & immunity - health · 2024Review
- Microglial AKAP8L: a key mediator in diabetes-associated cognitive impairment via autophagy inhibition and neuroinflammation triggering.Journal of neuroinflammation · 2024Article
- Polyphyllin I alleviates neuroinflammation after cerebral ischemia-reperfusion injury via facilitating autophagy-mediated M2 microglial polarization.Molecular medicine (Cambridge, Mass.) · 2024Article
- Chitosan-Rapamycin Carbon Dots Alleviate Glaucomatous Retinal Injury by Inducing Autophagy to Promote M2 Microglial Polarization.International journal of nanomedicine · 2024Article
- Research progress in the mechanism of acupuncture regulating microglia in the treatment of Alzheimer's disease.Frontiers in neuroscience · 2024Review
- Molecular Regulation Mechanism of Microglial Autophagy in the Pathology of Alzheimer's Disease.Aging and disease · 2023Review
- Mesenchymal stromal cell-derived secretome-based therapy for neurodegenerative diseases: overview of clinical trials.Stem cell research & therapy · 2023Review
- Autophagy Balances Neuroinflammation in Alzheimer's Disease.Cellular and molecular neurobiology · 2023Review
- Increased neutrophils in inflammatory bowel disease accelerate the accumulation of amyloid plaques in the mouse model of Alzheimer's disease.Inflammation and regeneration · 2023Article
- 1,25-Dihydroxy Vitamin DBioMed research international · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-4 plays an important protective role in Alzheimer's disease by regulating microglial phenotype, phagocytosis of amyloid-β, and secretion of anti-inflammatory and neurotrophic cytokines. Recently, increasing evidence has suggested that autophagy regulates innate immunity by affecting M1/M2 polarization of microglia/macrophages. However, the role of interleukin-4 in microglial autophagy is unknown. In view of this, BV2 microglia were treated with 0, 10, 20 or 50 ng/mL interleukin-4 for 24, 48, or 72 hours. Subsequently, light chain 3-II and p62 protein expression levels were detected by western blot assay. BV2 microglia were incubated with interleukin-4 (20 ng/mL, experimental group), 3-methyladenine (500 μM, autophagy inhibitor, negative control group), rapamycin (100 nM, autophagy inductor, positive control group), 3-methyladenine + interleukin-4 (rescue group), or without treatment for 24 hours, and then exposed to amyloid-β (1 μM, model group) or vehicle control (control) for 24 hours. LC3-II and p62 protein expression levels were again detected by western blot assay. In addition, expression levels of multiple markers of M1 and M2 phenotype were assessed by real-time fluorescence quantitative polymerase chain reaction, while intracellular and supernatant amyloid-β protein levels were measured by enzyme-linked immunosorbent assay. Our results showed that interleukin-4 induced microglial autophagic flux, most significantly at 20 ng/mL for 48 hours. Interleukin-4 pretreated microglia inhibited blockade of amyloid-β-induced autophagic flux, and promoted amyloid-β uptake and degradation partly through autophagic flux, but inhibited switching of amyloid-β-induced M1 phenotype independent on autophagic flux. These results indicate that interleukin-4 pretreated microglia increases uptake and degradation of amyloid-β in a process partly mediated by autophagy, which may play a protective role against Alzheimer's disease.
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.