ReviewFrontiers in immunology2025
Super-enhancers in immune system regulation: mechanisms, pathological reprogramming, and therapeutic opportunities.
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.
- From cell to disease: Regulatory networks and mechanisms of super‑enhancers in aging (Review).Molecular medicine reports · 2026Review
- Dissecting age-specific genetic architecture of vitiligo through integrative Post-GWAS analysis.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Super-enhancers (SEs) are dynamic chromatin structures that function as epigenetic hubs, orchestrating cell-type-specific transcriptional programs crucial for immune cell differentiation, functional specialization, and adaptive responses. These enhancer clusters integrate transcription factor (TF) networks, chromatin-modifying signals, and three-dimensional genome organization to govern lineage commitment, effector function acquisition, and metabolic reprogramming while enabling plasticity in response to environmental cues. SEs exhibit spatiotemporal regulatory properties, such as chromatin looping, phase-separated condensate formation, and stimulus-driven enhancer-promoter rewiring, all of which stabilize transcriptional outputs vital for immune homeostasis. Pathological dysregulation of SEs disrupts immune tolerance and amplifies aberrant transcriptional circuits, contributing to immune-mediated diseases marked by chronic inflammation, autoimmunity, or malignancy. Emerging therapeutic strategies targeting SE-associated components show promise in dismantling pathogenic enhancer networks through CRISPR-based editing, small-molecule inhibitors, and proteolysis-targeting chimeras(PROTACs). However, challenges remain in achieving therapeutic specificity amidst the dynamic reorganization of SEs and ensuring cell-type-selective delivery. By providing insights into SE-driven chromatin dynamics and transcriptional control in health and disease, this review focuses on two central questions: whether SEs causally drive immune cell fate decisions, and how they function within shared core transcriptional regulatory networks across cancer, infection, and autoimmune diseases. Future advances in multi-omics profiling, single-cell resolution analyses, and combinatorial therapeutic strategies will be critical for translating SE biology into precision interventions that restore immune equilibrium in dysregulated conditions.
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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.