ArticleJournal of leukocyte biology2014
Analysis of the transcriptional networks underpinning the activation of murine macrophages by inflammatory mediators.
Article in Journal of leukocyte biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 53 citations in OpenAlex.
- Multi-level transcriptional control of specific macrophage responses.The EMBO journal · 2026Review
- High-throughput label-free single-cell proteomics enabled by multicolumn NanoLC.Nature communications · 2026Article
- High-Throughput Label-free Single-Cell Proteomics Enabled by Multicolumn NanoLC with a 5-min Cycle Time.Research square · 2025Article
- Lyn expression in macrophages promotes TLR activation and restricts proliferation in an isoform-independent manner.Journal of leukocyte biology · 2025Article
- Quantitative Analysis of Monocyte-Derived Macrophage NFκB Signaling in Cancer Co-culture Models Using Luciferase-Based Biosensing.Cellular and molecular bioengineering · 2025Article
- Identification of novel protein biomarkers of macrophage polarization using comparative proteomic analyses of murine primary macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Integrating genetic variation with deep learning provides context for variants impacting transcription factor binding during embryogenesis.Genome research · 2025Article
- Article
- Transcriptomic Analysis of Macrophage Polarization Protocols: Vitamin DBiomedicines · 2023Article
- Dexamethasone impairs the expression of antimicrobial mediators in lipopolysaccharide-activated primary macrophages by inhibiting both expression and function of interferon β.Frontiers in immunology · 2023Article
- Article
- Mechanoimmunology: Are inflammatory epigenetic states of macrophages tuned by biophysical factors?APL bioengineering · 2022Review
- P. aeruginosa type III and type VI secretion systems modulate early response gene expression in type II pneumocytes in vitro.BMC genomics · 2022Article
- Proteome Profiling of PMJ2-R and Primary Peritoneal Macrophages.International journal of molecular sciences · 2021Article
- Dermal bacterial LPS-stimulation reduces susceptibility to intradermal Trypanosoma brucei infection.Scientific reports · 2021Article
- Cross Talk Between Macrophages and Cancer Cells in the Bone Metastatic Environment.Frontiers in endocrinology · 2021Review
- High Dose IFN-Frontiers in immunology · 2021Article
- Transcriptional profiling of murine macrophages stimulated with cartilage fragments revealed a strategy for treatment of progressive osteoarthritis.Scientific reports · 2020Article
- Type-I interferons in atherosclerosis.The Journal of experimental medicine · 2020Review
- Species-Specificity of Transcriptional Regulation and the Response to Lipopolysaccharide in Mammalian Macrophages.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
- Commented on by
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Macrophages respond to the TLR4 agonist LPS with a sequential transcriptional cascade controlled by a complex regulatory network of signaling pathways and transcription factors. At least two distinct pathways are currently known to be engaged by TLR4 and are distinguished by their dependence on the adaptor molecule MyD88. We have used gene expression microarrays to define the effects of each of three variables--LPS dose, LPS versus IFN-β and -γ, and genetic background--on the transcriptional response of mouse BMDMs. Analysis of correlation networks generated from the data has identified subnetworks or modules within the macrophage transcriptional network that are activated selectively by these variables. We have identified mouse strain-specific signatures, including a module enriched for SLE susceptibility candidates. In the modules of genes unique to different treatments, we found a module of genes induced by type-I IFN but not by LPS treatment, suggesting another layer of complexity in the LPS-TLR4 signaling feedback control. We also observe that the activation of the complement system, in common with the known activation of MHC class 2 genes, is reliant on IFN-γ signaling. Taken together, these data further highlight the exquisite nature of the regulatory systems that control macrophage activation, their likely relevance to disease resistance/susceptibility, and the appropriate response of these cells to proinflammatory stimuli.
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.