ArticleBrain sciences2021
Differential Cytokine-Induced Responses of Polarized Microglia.
Article in Brain sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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
25 citing papers in PubMed, 38 citations in OpenAlex.
- Oxidative stress and inflammation in neurodegenerative disorders.Archives of toxicology · 2026Review
- Alzheimer's disease: from molecular pathways to therapies.Molecular biomedicine · 2026Review
- Anti-Inflammatory and Synaptic Protective Effects of TNF-α Inactivation in the MDX Mouse Model.Current issues in molecular biology · 2026Article
- Interleukin-6 as a keystone cytokine in experimental rat models of chemotherapy-induced peripheral neurotoxicity.Scientific reports · 2026Article
- The Mechanism of Ultrasonic Lysis ofCells · 2026Article
- Neuroinflammatory and Redox Responses in a Rat Model of NTG-Induced Migraine.International journal of molecular sciences · 2025Article
- Improvement of Parkinson's Disease Symptoms by Butylphthalide Through Modulation of Microglial Activation.Neuromolecular medicine · 2025Article
- Resolvin D1 suppresses inflammation in human fibroblast-like synoviocytes via the p-38, NF-κB, and AKT signaling pathways.In vitro cellular & developmental biology. Animal · 2025Article
- Tofacitinib prevents depressive-like behaviors through decreased hippocampal microgliosis and increased BDNF levels in both LPS-induced and CSDS-induced mice.Acta pharmacologica Sinica · 2025Article
- Article
- Bidirectional crosstalk between microglia and serotonin signaling in neuroinflammation and CNS disorders.Frontiers in immunology · 2025Review
- Roles of 4'-International journal of molecular sciences · 2024Article
- The Role of Pyroptosis and Autophagy in the Nervous System.Molecular neurobiology · 2024Review
- Effects and mechanisms of APP and its cleavage product Aβ in the comorbidity of sarcopenia and Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Thrombin-Induced Microglia Activation Modulated through Aryl Hydrocarbon Receptors.International journal of molecular sciences · 2023Article
- The role of signaling crosstalk of microglia in hippocampus on progression of ageing and Alzheimer's disease.Journal of pharmaceutical analysis · 2023Article
- TheBrain sciences · 2023Article
- Microglia and Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Mechanism and Regulation of Microglia Polarization in Intracerebral Hemorrhage.Molecules (Basel, Switzerland) · 2022Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The role of select pro- and anti-inflammatory mediators in driving microglial cell polarization into classically (M1), or alternatively, (M2) activated states, as well as the subsequent differential responses of these induced phenotypes, was examined. Expression of PD-L1, MHC-II, MHC-I, arginase 1 (Arg-1), and inducible nitric oxide synthase (iNOS) was assessed using multi-color flow cytometry. We observed that both pro- and anti-inflammatory mediators induced PD-L1 expression on non-polarized microglia. Moreover, IFN-γ stimulated significant MHC class I and II expression on these cells. Interestingly, we observed that only IL-4 treatment induced Arg-1 expression, indicating M2 polarization. These M2 cells were refractory to subsequent depolarization and maintained their alternatively activated state. Furthermore, PD-L1 expression was significantly induced on these M2-polarized microglia after treatment with pro-inflammatory mediators, but not anti-inflammatory cytokines. In addition, we observed that only LPS induced iNOS expression in microglial cells, indicating M1 polarization. Furthermore, IFN-γ significantly increased the percentage of M1-polarized microglia expressing iNOS. Surprisingly, when these M1-polarized microglia were treated with either IL-6 or other anti-inflammatory cytokines, they returned to their non-polarized state, as demonstrated by significantly reduced expression of iNOS. Taken together, these results demonstrate differential responses of microglial cells to mediators present in dissimilar microenvironments.
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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 Socratic graph.