ArticleNature communications2021
Epigenetically regulated digital signaling defines epithelial innate immunity at the tissue level.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The trial behind it
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Heritable single-cell gene expression states shape functional variability in innate immune responses.bioRxiv : the preprint server for biology · 2026Article
- Review
- MemorySeq identifies heritable epigenetic phenotypes that initiate cell culture stress tolerance in CHO cells.iScience · 2025Article
- Lineage memory shapes viral resistance barriers in human skin.bioRxiv : the preprint server for biology · 2025Article
- Stochastic gene expression in proliferating cells: Differing noise intensity in single-cell and population perspectives.PLoS computational biology · 2025Article
- Non-genetic differences underlie variability in proliferation among esophageal epithelial clones.PLoS computational biology · 2024Article
- Article
- Review
- Stochastic Gene Expression in Proliferating Cells: Differing Noise Intensity in Single-Cell and Population Perspectives.bioRxiv : the preprint server for biology · 2024Article
- CDK4/6 activity is required during GScience (New York, N.Y.) · 2024Article
- Unraveling IFN-I response dynamics and TNF crosstalk in the pathophysiology of systemic lupus erythematosus.Frontiers in immunology · 2024Article
- Article
- Article
- Revising immune cell coordination: Origins and importance of single-cell variation.European journal of immunology · 2022Review
- Review
- Emerging roles for endogenous retroviruses in immune epigenetic regulation.Immunological reviews · 2022Review
- Probing transient memory of cellular states using single-cell lineages.Frontiers in microbiology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
To prevent damage to the host or its commensal microbiota, epithelial tissues must match the intensity of the immune response to the severity of a biological threat. Toll-like receptors allow epithelial cells to identify microbe associated molecular patterns. However, the mechanisms that mitigate biological noise in single cells to ensure quantitatively appropriate responses remain unclear. Here we address this question using single cell and single molecule approaches in mammary epithelial cells and primary organoids. We find that epithelial tissues respond to bacterial microbe associated molecular patterns by activating a subset of cells in an all-or-nothing (i.e. digital) manner. The maximum fraction of responsive cells is regulated by a bimodal epigenetic switch that licenses the TLR2 promoter for transcription across multiple generations. This mechanism confers a flexible memory of inflammatory events as well as unique spatio-temporal control of epithelial tissue-level immune responses. We propose that epigenetic licensing in individual cells allows for long-term, quantitative fine-tuning of population-level responses.
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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.