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Naik, S., Bouladoux, N., & Linehan, J. L. (2015). Commensal–dendritic-cell interaction specifies a unique protective skin immune signature. Nature, 520(7545), 104–108. Added by: Dr. Enrique Feoli (07/11/2023, 14:39) Last edited by: Dr. Enrique Feoli (07/11/2023, 14:46) |
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| Resource type: Journal Article DOI: 10.1038/nature14052 ID no. (ISBN etc.): 0028-0836 BibTeX citation key: Naik2015 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: Microbiota on immunity Creators: Bouladoux, Linehan, Naik Collection: Nature |
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| Abstract |
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The skin represents the primary interface between the host and the environment. This organ is also home to trillions of microorganisms that play an important role in tissue homeostasis and local immunity–. Skin microbial communities are highly diverse and can be remodelled over time or in response to environmental challenges–. How, in the context of this complexity, individual commensal microorganisms may differentially modulate skin immunity and the consequences of these responses for tissue physiology remains unclear. Here we show that defined commensals dominantly affect skin immunity and identify the cellular mediators involved in this specification. In particular, colonization with Staphylococcus epidermidis induces IL-17A+ CD8+ T cells that home to the epidermis, enhance innate barrier immunity and limit pathogen invasion. Commensal-specific T-cell responses result from the coordinated action of skin-resident dendritic cell subsets and are not associated with inflammation, revealing that tissue-resident cells are poised to sense and respond to alterations in microbial communities. This interaction may represent an evolutionary means by which the skin immune system uses fluctuating commensal signals to calibrate barrier immunity and provide heterologous protection against invasive pathogens. These findings reveal that the skin immune landscape is a highly dynamic environment that can be rapidly and specifically remodelled by encounters with defined commensals, findings that have profound implications for our understanding of tissue-specific immunity and pathologies.
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| Notes |
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a, Relative abundance of bacterial phyla in mouse skin 14 and 180 days after S. epidermidis topical application. Each bar represents the percentage of sequences in operational taxonomic units (OTUs) assigned to each phylum for an individual mouse. Ctrl, control. b, Enumeration of colony-forming units (c.f.u.) from the ears after S. epidermidis application (n = 5–10 per group). c, IFN-γ and IL-17A production by skin, lung or gut effector (CD45+ TCRβ+ Foxp3−) T cells in unassociated (control) and S. epidermidis (S. epi.)-associated mice at day 14. d, Absolute numbers of skin IFN-γ+ or IL-17A+ effector T cells in unassociated mice (control, n = 3) and mice topically associated with live (S. epi., n = 4) or heat-killed (HK S. epi., n = 4) S. epidermidis at day 14. e, Representative images and histopathological comparison of the ear pinnae of unassociated (control), topically associated (topical) or intradermally inoculated (intradermal) mice at day 7. Scale bars, 250 µm. f, g, Frequencies and absolute numbers of skin IFN-γ+ or IL-17A+ effector T cells after topical application (n = 4) or intradermal inoculation (n = 4–5) of S. epidermidis. h, IFN-γ and IL-17A production by skin effector T cells in unassociated and S. epidermidis-associated mice at different time points. Results are representative of 2–3 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 as calculated by Student’s t-test. Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli |
