ArticleNature2017
Inflammatory memory sensitizes skin epithelial stem cells to tissue damage.
Article in Nature, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 420 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
420 citing papers in PubMed.
- The epigenetic-metabolic axis of trained immunity: dual roles in disease pathogenesis and intervention.Journal of molecular medicine (Berlin, Germany) · 2026Review
- IL-33 as a boundary-tissue state-transfer signal: a Reader-Alarmin-Effector architecture linking CNS and skin.Brain, behavior, & immunity - health · 2026Review
- The effects of IFNγ on tissue physiology through structural cells.Nature reviews. Immunology · 2026Review
- Metabolomics of in vivo inflammation identifies soluble sialic acid as a conserved myeloid-cell metabolite.The Journal of biological chemistry · 2026Article
- The theory of the inflammatory ecosystem.Science China. Life sciences · 2026Review
- Trained immunity links hematopoietic stem cell aging to aging-associated inflammation.Nature aging · 2026Article
- Rewiring Atopic Dermatitis: Alarmin Cytokines at the Core of Barrier-Immune-Neuro-Microbiome Networks.Clinical reviews in allergy & immunology · 2026Review
- Emergency granulopoiesis and innate immune memory in inflammatory bowel disease.Trends in immunology · 2026Review
- Epithelial-Dermal Immune Memory: TrackingInternational journal of molecular sciences · 2026Review
- An immune-poised state of human bronchial epithelial cells mediates defense against RSV in adults.Nature communications · 2026Article
- The basal cell state maintains pancreatic cancers by controlling an immunosuppressive circuit.bioRxiv : the preprint server for biology · 2026Article
- Loss of tissue-state plasticity: a conceptual framework for age-associated regenerative failure.Inflammation and regeneration · 2026Review
- Metabolomics ofbioRxiv : the preprint server for biology · 2026Article
- Article
- RUNX1 is a mediator of fibrotic activation and epigenetic memory in lung fibroblasts.American journal of respiratory cell and molecular biology · 2026Article
- Omics-based decoding of molecular and metabolic crosstalk in the skin barrier ecosystem.Cell death and differentiation · 2026Review
- Epigenetic mechanisms of inflammatory memory in the central nervous system.Nature immunology · 2026Review
- Guarding epithelial integrity: origins of adaptive immunity and cancer immunosurveillance over time and space.Journal for immunotherapy of cancer · 2026Review
- Article
- Trained immunity modulators: A new frontier in immunoregulation and disease intervention.Journal of advanced research · 2026Review
360 more citing papers are in PubMed but not listed here.
Corrections and comments
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- Erratum issued
Authors and funding
10 authors.
Funding
Abstract
The skin barrier is the body's first line of defence against environmental assaults, and is maintained by epithelial stem cells (EpSCs). Despite the vulnerability of EpSCs to inflammatory pressures, neither the primary response to inflammation nor its enduring consequences are well understood. Here we report a prolonged memory to acute inflammation that enables mouse EpSCs to hasten barrier restoration after subsequent tissue damage. This functional adaptation does not require skin-resident macrophages or T cells. Instead, EpSCs maintain chromosomal accessibility at key stress response genes that are activated by the primary stimulus. Upon a secondary challenge, genes governed by these domains are transcribed rapidly. Fuelling this memory is Aim2, which encodes an activator of the inflammasome. The absence of AIM2 or its downstream effectors, caspase-1 and interleukin-1β, erases the ability of EpSCs to recollect inflammation. Although EpSCs benefit from inflammatory tuning by heightening their responsiveness to subsequent stressors, this enhanced sensitivity probably increases their susceptibility to autoimmune and hyperproliferative disorders, including cancer.
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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.