ArticleCell host & microbe2019
Toxin-Triggered Interleukin-1 Receptor Signaling Enables Early-Life Discrimination of Pathogenic versus Commensal Skin Bacteria.
Article in Cell host & microbe, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 93 citations in OpenAlex.
- Regulatory T cells in the skin: Origin, function, and plasticity.JID innovations : skin science from molecules to population health · 2026Review
- Beyond the skin barrier: commensalbioRxiv : the preprint server for biology · 2026Article
- The human skin microbiome: from metagenomes to therapeutics.Nature reviews. Microbiology · 2025Review
- Restoration of the human skin microbiome following immune recovery after hematopoietic stem cell transplantation.Cell host & microbe · 2025Article
- Engineered Tissue Models to Decode Host-Microbiota Interactions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Staphylococcus aureus promotes strain-dependent immunopathology during cutaneous leishmaniasis through induction of IL-1β.Cell reports · 2025Article
- Skin Microbiome and Radiation-Induced Skin Injury: Unraveling the Relationship, Mechanisms, and Therapeutic Implications.International journal of molecular sciences · 2025Review
- Conversation between skin microbiota and the host: from early life to adulthood.Experimental & molecular medicine · 2025Review
- Epsilon-polylysine microneedle potentiating MXene-mediated photothermal ablation for combating antibiotic-resistant bacterial infections.Materials today. Bio · 2025Article
- Crosstalk Between the Skin Environment and Microbial Community in Immune-Related Skin Diseases.Clinical reviews in allergy & immunology · 2025Review
- Skin microbiome and dermatologic disorders.The Journal of clinical investigation · 2025Review
- CommensalFrontiers in immunology · 2025Article
- Beneficial perspective onFrontiers in immunology · 2025Review
- Microbial Dysbiosis in the Skin Microbiome and Its Psychological Consequences.Microorganisms · 2024Review
- Tissue resident cells differentiate S. aureus from S. epidermidis via IL-1β following barrier disruption in healthy human skin.PLoS pathogens · 2024Article
- CCR5 promotes the migration of pathological CD8+ T cells to the leishmanial lesions.PLoS pathogens · 2024Article
- Genome-wide transcription response ofFrontiers in microbiology · 2024Article
- Towards sustainable antimicrobial therapies forSustainable microbiology · 2024Review
- The inner elbow skin microbiome containsMicrobiome research reports · 2024Article
- Article
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13 authors at 2 institutions in 1 country.
Funding
Abstract
The host must develop tolerance to commensal microbes and protective responses to infectious pathogens, yet the mechanisms enabling a privileged relationship with commensals remain largely unknown. Skin colonization by commensal Staphylococcus epidermidis facilitates immune tolerance preferentially in neonates via induction of antigen-specific regulatory T cells (Tregs). Here, we demonstrate that this tolerance is not indiscriminately extended to all bacteria encountered in this early window. Rather, neonatal colonization by Staphylococcus aureus minimally enriches for antigen-specific Tregs and does not prevent skin inflammation upon later-life exposure. S. aureus α-toxin contributes to this response by stimulating myeloid cell production of IL-1β, which limits S. aureus-specific Tregs. Loss of α-toxin or the IL-1 receptor increases Treg enrichment, whereas topical application of IL-1β or α-toxin diminishes tolerogenic responses to S. epidermidis. Thus, the preferential activation of a key alarmin pathway facilitates early discrimination of microbial "foe" from "friend," thereby preventing tolerance to a common skin pathogen.
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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.