ArticleFrontiers in immunology2022
Activation of LXR Nuclear Receptors Impairs the Anti-Inflammatory Gene and Functional Profile of M-CSF-Dependent Human Monocyte-Derived Macrophages.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- The Multifaceted Roles of Macrophages in Rheumatoid Arthritis: From Cytokine Networks to the Discovery of Novel Subsets.International journal of molecular sciences · 2026Review
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- A single-cell atlas of RNA alternative splicing in the glioma-immune ecosystem.Genome biology · 2025Article
- Inhibition of LXR Signaling in Human Foam Cells Impairs Macrophage-to-Endothelial Cell Cross Talk and Promotes Endothelial Cell Inflammation.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Reprogramming of GM-CSF-dependent alveolar macrophages through GSK3 activity modulation.eLife · 2025Article
- Exploring the Roles of Liver X Receptors in Lipid Metabolism and Immunity in Atherosclerosis.Biomolecules · 2025Review
- Active LXR signaling, coupled with elevated mitochondrial and glycolytic metabolism contributes to GM-CSF-induced trained immunity.Frontiers in immunology · 2025Article
- Crosstalk between lipid metabolism and macrophages in atherosclerosis: therapeutic potential of natural products.Frontiers in cardiovascular medicine · 2025Review
- Ovine macrophage identity and plasticity: novel insights into CSF-driven polarization and species-specific responses.Frontiers in immunology · 2025Article
- Macrophage re-programming by JAK inhibitors relies on MAFB.Cellular and molecular life sciences : CMLS · 2024Article
- Ginsenoside F2 Restrains Hepatic Steatosis and Inflammation by Altering the Binding Affinity of Liver X Receptor Coregulators.Journal of ginseng research · 2024Article
- Impact of Lipid Metabolism on Macrophage Polarization: Implications for Inflammation and Tumor Immunity.International journal of molecular sciences · 2023Review
- Inhibition of LXR controls the polarization of human inflammatory macrophages through upregulation of MAFB.Cellular and molecular life sciences : CMLS · 2023Article
- Liver X receptors and estrogen receptor β, two players in a rare subtype of NSCLC.International journal of biological sciences · 2023Article
- Dynamic polarization of tumor-associated macrophages and their interaction with intratumoral T cells in an inflamed tumor microenvironment: from mechanistic insights to therapeutic opportunities.Frontiers in immunology · 2023Review
- Hepatic macrophage mediated immune response in liver steatosis driven carcinogenesis.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver X Receptors (LXR) control cholesterol metabolism and exert anti-inflammatory actions but their contribution to human macrophage polarization remains unclear. The LXR pathway is enriched in pro-inflammatory macrophages from rheumatoid arthritis as well as in tumors-associated macrophages from human tumors. We now report that LXR activation inhibits the anti-inflammatory gene and functional profile of M-CSF-dependent human macrophages, and prompts the acquisition of a pro-inflammatory gene signature, with both effects being blocked by an LXR inverse agonist. Mechanistically, the LXR-stimulated macrophage polarization shift correlates with diminished expression of MAFB and MAF, which govern the macrophage anti-inflammatory profile, and with enhanced release of activin A. Indeed, LXR activation impaired macrophage polarization in response to tumor-derived ascitic fluids, as well as the expression of MAF- and MAFB-dependent genes. Our results demonstrate that LXR activation limits the anti-inflammatory human macrophage polarization and prompts the acquisition of an inflammatory transcriptional and functional profile.
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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.