SynthesisJournal of neuroinflammation2022
The cytokines interleukin-6 and interferon-α induce distinct microglia phenotypes.
Synthesis in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 77 citations in OpenAlex.
- Predicting the Beneficial Effects of Cognitive Stimulation and Transcranial Direct Current Stimulation in Amnestic Mild Cognitive Impairment with Clinical, Inflammation, and Human Microglia Exposed to Serum as Potential Markers: A Double-Blind Placebo-Controlled Randomized Clinical Trial.International journal of molecular sciences · 2025Trial
- Article
- BMI-genome interactions regulate global gene expression with emphasis in brain and gut.Cell genomics · 2026Article
- Azetidine-2-carboxylic acid-induced oligodendrogliopathy in vitro and the pathogenesis of multiple sclerosis.Journal of neuropathology and experimental neurology · 2026Article
- Chronic central-targeted Interleukin-6 overexpression promotes hippocampal and cortical neuropathology in the Tg2576 mouse model of Alzheimer's disease.Alzheimer's research & therapy · 2026Article
- Type-1 interferons associated with microglial-mediated neuroinflammation in Alzheimer's disease.Journal of neuroinflammation · 2026Review
- Molecular and Mechanistic Divergence of Seizures in Pediatric Acute Lymphoblastic Leukemia: CNS Infiltration Versus Chemotherapy-Induced Neurotoxicity.International journal of molecular sciences · 2026Review
- From Polyphenols to Prodrugs: Bridging the Blood-Brain Barrier with Nanomedicine and Neurotherapeutics.International journal of molecular sciences · 2026Review
- Biomarkers for satralizumab treatment in neuromyelitis optica spectrum disorders: a prospective case series.BMC neurology · 2026Article
- Oxymatrine-associated protection in an MPTP mouse model is accompanied by increased miR-141-3p and reduced HMGB1.Frontiers in molecular neuroscience · 2026Article
- NLRC5-Mediated Epigenetic and Proteomic Regulation of Microglial Panoptosis Drives Neuroinflammation in Multiple Sclerosis.Molecular neurobiology · 2025Article
- Article
- Epigenetics and immunology: Under-recognized aspects of suicidality.World journal of psychiatry · 2025Review
- Microglial deficiency in the ATRX chromatin remodeler elicits a viral mimicry immune response that impacts neuronal function and behavior.PLoS biology · 2025Article
- Behavioral assessment and gene expression changes in a mouse model with dysfunctional STAT1 signaling.Cell communication and signaling : CCS · 2025Article
- Regulatory T Cell in Kidney Transplant: The Future of Cell Therapy?Antibodies (Basel, Switzerland) · 2025Review
- Microglial pro-inflammatory mechanisms induced by monomeric C-reactive protein are counteracted by soluble epoxide hydrolase inhibitors.International immunopharmacology · 2025Article
- Interleukin-6 produces behavioral deficits in pre-pubescent mice independent of neuroinflammation.Brain, behavior, and immunity · 2025Article
- Type I interferons regulate nitric oxide production inFrontiers in immunology · 2025Article
- Brain penetration of peripheral extracellular vesicles from Alzheimer's patients and induction of microglia activation.Journal of extracellular biology · 2025Article
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 2 institutions in 2 countries.
Funding
Abstract
backgroundElevated production of the cytokines interleukin (IL)-6 or interferon (IFN)-α in the central nervous system (CNS) is implicated in the pathogenesis of neurological diseases such as neuromyelitis optica spectrum disorders or cerebral interferonopathies, respectively. Transgenic mice with CNS-targeted chronic production of IL-6 (GFAP-IL6) or IFN-α (GFAP-IFN) recapitulate important clinical and pathological features of these human diseases. The activation of microglia is a prominent manifestation found both in the human diseases and in the transgenic mice, yet little is known about how this contributes to disease pathology.
methodsHere, we used a combination of ex vivo and in situ techniques to characterize the molecular, cellular and transcriptomic phenotypes of microglia in GFAP-IL6 versus GFAP-IFN mice. In addition, a transcriptomic meta-analysis was performed to compare the microglia response from GFAP-IL6 and GFAP-IFN mice to the response of microglia in a range of neurodegenerative and neuroinflammatory disorders.
resultsWe demonstrated that microglia show stimulus-specific responses to IL-6 versus IFN-α in the brain resulting in unique and extensive molecular and cellular adaptations. In GFAP-IL6 mice, microglia proliferated, had shortened, less branched processes and elicited transcriptomic and molecular changes associated with phagocytosis and lipid processing. In comparison, microglia in the brain of GFAP-IFN mice exhibited increased proliferation and apoptosis, had larger, hyper-ramified processes and showed transcriptomic and surface marker changes associated with antigen presentation and antiviral response. Further, a transcriptomic meta-analysis revealed that IL-6 and IFN-α both contribute to the formation of a core microglia response in animal models of neurodegenerative and neuroinflammatory disorders, such as Alzheimer's disease, tauopathy, multiple sclerosis and lipopolysaccharide-induced endotoxemia.
conclusionsOur findings demonstrate that microglia responses to IL-6 and IFN-α are highly stimulus-specific, wide-ranging and give rise to divergent phenotypes that modulate microglia responses in neuroinflammatory and neurodegenerative diseases.
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.