ReviewFrontiers in immunology2025
Macrophage-tregs crosstalk: the "hub" of the immune network in MASLD.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- Immune Determinants of MASLD Progression: From Immunometabolic Reprogramming to Fibrotic Transformation.Biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a globally prevalent metabolic disorder with a high average worldwide prevalence. It occurs more frequently in men than in women, and its incidence increases with age. MASLD can progressively advance to liver fibrosis, cirrhosis, and even hepatocellular carcinoma, while also elevating the risk of cardiovascular, renal, and other systemic diseases. Its pathological progression is closely associated with dysregulation of the hepatic immune microenvironment, in which aberrant crosstalk between Macrophages (Mø) and regulatory T cells (Tregs) serves as a central driving mechanism. Under physiological conditions, liver-resident Macrophages (Kupffer cells, KCs) and Tregs maintain immune homeostasis through a "complementary origin-spatial co-localization-molecular crosstalk" mechanism. In MASLD, KCs numbers decline while monocyte-derived Macrophages (MDMs) are abnormally recruited, giving rise to Macrophages with distinct phenotypes. Tregs influence the classical phenotypic differentiation of Macrophages. However, dynamic alterations in Treg abundance exhibit a "double-edged sword" effect. The disrupted crosstalk between KCs and Tregs involves dysregulated chemokine networks [e.g., c-x-c motif chemokine ligand 9 (CXCL9), c-c motif chemokine ligand 2 (CCL2)], cytokine interactions [e.g., interleukin-1β (IL-1β), transforming growth factor- Beta (TGF-β)], and signaling pathways such as beta-catenin (β-catenin) and notch homolog 1 (Notch1). Collectively, these alterations drive disease progression from steatosis to hepatitis and fibrosis. This review systematically summarizes the physiological mechanisms underlying Macrophages -Tregs crosstalk, its pathological dysregulation in MASLD, and the associated molecular networks, while proposing targeted therapeutic strategies based on disease stage.
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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 Socratic graph.