ArticleProtein & cell2018
IL-23-induced macrophage polarization and its pathological roles in mice with imiquimod-induced psoriasis.
Article in Protein & cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
101 citing papers in PubMed, 2 syntheses or guidelines pooled it, 173 citations in OpenAlex.
- Macrophages in psoriasis: a bibliometric analysis of research trends, knowledge gaps, and future directions (2015-2024).Frontiers in medicine · 2026Pooled it
- A Systematic Review with Meta-Analysis of Comparative Efficacy and Safety of Risankizumab and Ustekinumab for Psoriasis Treatment.Journal of immunology research · 2022Pooled it
- The impact of biologics targeting the IL-17 and IL-23 pathways on metabolic indicators in plaque psoriasis.Archives of dermatological research · 2025Trial
- Molecular Signature and miRNA Pattern of CD4 + T Lymphocytes in Plaque Psoriasis.Clinical reviews in allergy & immunology · 2026Review
- The role of non-coding RNAs derived from macrophage exosomes in cardiovascular diseases.The Journal of physiology · 2026Review
- Macrophage INSIG1 deficiency drives psoriasiform dermatitis via the SREBP2-STAT1 axis.Nature communications · 2026Article
- Beyond polarization: a receptor-centered framework for macrophage function and therapy in skin diseases.Clinical and experimental medicine · 2026Review
- The multifaceted role of NF-κB signaling in psoriasis: from inflammatory amplification to epidermal remodeling.Frontiers in immunology · 2026Review
- A 76-week real-world multidimensional analysis of guselkumab in moderate to severe plaque psoriasis: a retrospective cohort study based on Chinese clinical practice standards.Frontiers in immunology · 2026Article
- Systemic CSF1R Targeting Depletes Pathogenic MPS Bubs and Ameliorates Psoriasis via PPARα-mediated Resolution.Theranostics · 2026Article
- Neural regulatory networks: challenges and opportunities in the treatment of psoriasis.Frontiers in immunology · 2026Review
- Macrophage-Driven Bidirectional Exacerbation in Psoriasis-Atherosclerosis Comorbidity: Insights From a Novel Mouse Model.Mediators of inflammation · 2026Article
- Human urine-derived stem cells alleviate psoriasis by suppressing JAK2/STAT3 pathway-mediated macrophage polarization.Stem cell research & therapy · 2025Article
- LZTR1 regulates epithelial MHC-I expression via NF-κB1 to modulate CD8Cell discovery · 2025Article
- The Therapeutic Potential of Extracellular Vesicles in Psoriasis Treatment: Mechanisms, Applications, and Prospects.International journal of molecular sciences · 2025Review
- Macrophagic Ym1 orchestrates γδT cell-derived IL-17 production and keratinocyte functionality to mediate psoriasis-like skin inflammation.Communications biology · 2025Article
- Niclosamide Alleviated Skin Inflammation and Restored the Balance between Effector and Regulatory T Cells in Skin.Biomolecules & therapeutics · 2025Article
- Insights for lncH19, miR-9, and miR-146a expression levels and their cross-talk with pro-inflammatory cytokines, copeptin, and neopterin profile in type 1 diabetic cardiomyopathy.Molecular biology reports · 2025Article
- Hydrogen-bonded organic framework for regulating pathogenic autoantigen and oxidative stress in psoriasis treatment.National science review · 2025Article
- Decoding Macrophage Dynamics: A Pathway to Understanding and Treating Inflammatory Skin Diseases.International journal of molecular sciences · 2025Review
41 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages acquire distinct phenotypes during tissue stress and inflammatory responses. Macrophages are roughly categorized into two different subsets named inflammatory M1 and anti-inflammatory M2 macrophages. We herein identified a unique pathogenic macrophage subpopulation driven by IL-23 with a distinct gene expression profile including defined types of cytokines. The freshly isolated resting mouse peritoneal macrophages were stimulated with different cytokines in vitro, the expression of cytokines and chemokines were detected by microarray, real-time PCR, ELISA and multiple colors flow cytometry. Adoptive transfer of macrophages and imiquimod-induced psoriasis mice were used. In contrast to M1- and M2-polarized macrophages, IL-23-treated macrophages produce large amounts of IL-17A, IL-22 and IFN-γ. Biochemical and molecular studies showed that IL-23 induces IL-17A expression in macrophages through the signal transducer and activator of transcription 3 (STAT3)-retinoid related orphan receptor-γ T (RORγT) pathway. T-bet mediates the IFN-γ production in IL-23-treated macrophages. Importantly, IL-23-treated macrophages significantly promote the dermatitis pathogenesis in a psoriasis-like mouse model. IL-23-treated resting macrophages express a distinctive gene expression prolife compared with M1 and M2 macrophages. The identification of IL-23-induced macrophage polarization may help us to understand the contribution of macrophage subpopulation in Th17-cytokines-related pathogenesis.
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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 OpenQuestion graph.