ArticleScience advances2021
Microglia promote autoimmune inflammation via the noncanonical NF-κB pathway.
Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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.
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.
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Who cites it
38 citing papers in PubMed, 48 citations in OpenAlex.
- Mechanisms of Therapeutic Resistance and Recent Advances in Glioblastoma Treatment.Immunology and cell biology · 2026Review
- Forkhead box versus NF-κB hippocampal snRNA-seq profiles distinguish anti-Drebrin- and anti-GAD65-positive encephalitis.Journal of neuroinflammation · 2026Article
- Knowledge-guided contextual gene set analysis with large language models.Bioinformatics (Oxford, England) · 2026Article
- Tissue-Resident Macrophage-Derived E3 Ligase SMURF2 Restricts Autoimmune Inflammation by Mediating the Degradation of p-TBK1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Astrocyte-intrinsic signaling of chitinase-like protein CHI3L1 drives inflammation and amplifies demyelination in neuromyelitis optica.The Journal of clinical investigation · 2026Article
- Quantitative Analysis of Monocyte-Derived Macrophage NFκB Signaling in Cancer Co-culture Models Using Luciferase-Based Biosensing.Cellular and molecular bioengineering · 2025Article
- Gut-specific histamine 3 receptor signaling orchestrates microglia-dependent resolution of peripheral inflammation.The Journal of clinical investigation · 2025Article
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- Combined Bulk and Single-Cell Transcriptomic Analysis to Reveal the Potential Influences of Intestinal Inflammatory Disease on Multiple Sclerosis.Inflammation · 2025Article
- SiglecF Expressing Neutrophils Exacerbate Th17-Mediated Autoimmune Neuroinflammation.Immune network · 2025Article
- Targeting microglia-Th17 feed-forward loop to suppress autoimmune neuroinflammation.Journal of neuroinflammation · 2025Article
- Central TYK2 inhibition identifies TYK2 as a key neuroimmune modulator.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- From diagnosis to treatment: exploring the mechanisms underlying optic neuritis in multiple sclerosis.Journal of translational medicine · 2025Review
- The Dual Role of Microglia in Multiple Sclerosis and its Implications for Diagnostics and Repair.Current neuropharmacology · 2025Review
- CD4Frontiers in immunology · 2025Review
- Astrocyte-Derived Interleukin 11 Modulates Astrocyte-Microglia Crosstalk via Nuclear Factor-κB Signaling Pathway in Sepsis-Associated Encephalopathy.Research (Washington, D.C.) · 2025Article
- Deciphering T Cell Dynamics in Alzheimer's Disease Pathogenesis: Insights and Implications.Current neuropharmacology · 2025Review
- The impact of autoimmune diseases on delirium risk in critically ill patients: a propensity score matching multicenter analysis.Frontiers in medicine · 2025Article
- Microglia in the aged brain develop a hypoactive molecular phenotype after surgery.Journal of neuroinflammation · 2024Article
- Life history of a brain autoreactive T cell: From thymus through intestine to blood-brain barrier and brain lesion.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 3 countries.
Funding
Abstract
Microglia have been implicated in neuroinflammatory diseases, including multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). We demonstrate that microglia mediate EAE disease progression via a mechanism relying on the noncanonical nuclear factor kB (NF-κB) pathway. Microglia-specific deletion of the noncanonical NF-κB-inducing kinase (NIK) impairs EAE disease progression. Although microglial NIK is dispensable for the initial phase of T cell infiltration into the central nervous system (CNS) and EAE disease onset, it is critical for the subsequent CNS recruitment of inflammatory T cells and monocytes. Our data suggest that following their initial CNS infiltration, T cells activate the microglial noncanonical NF-κB pathway, which synergizes with the T cell-derived cytokine granulocyte-macrophage colony-stimulating factor to induce expression of chemokines involved in the second-wave of T cell recruitment and disease progression. These findings highlight a mechanism of microglial function that is dependent on NIK signaling and required for EAE disease progression.
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.