A wave of regulatory T cells into neonatal skin mediates tolerance to commensal microbes
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Summary The skin is a site of constant dialogue between the immune system and commensal bacteria. However, the molecular mechanisms that allow us to tolerate the presence of skin commensals without eliciting destructive inflammation are unknown. Using a model system to study the antigen-specific response to S. epidermidis, we demonstrated that skin colonization during a defined period of neonatal life was required to establish immune tolerance to commensal microbes. This crucial window was characterized by an abrupt influx of highly activated regulatory T (Treg) cells into neonatal skin. Selective inhibition of this Treg cell wave completely abrogated tolerance. Thus, the host-commensal relationship in the skin relied on a unique Treg cell population that mediated tolerance to bacterial antigens during a defined developmental window. This suggests that the cutaneous microbiome composition in neonatal life is crucial in shaping adaptive immune responses to commensals, and disrupting these interactions may have enduring health implications.
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Patients with AD frequently exhibit dysbiosis, manifested by a decrease in microbial diversity, with a skin environment that favors the growth of S. aureus, associated to an increase in skin pH and antimicrobial component deficiencies.
“Patients with AD frequently exhibit dysbiosis, manifested by a decrease in microbial diversity, with a skin environment that favors the growth of S. aureus, associated to an increase in skin pH and antimicrobial component deficiencies.97, 98, 99, 100, 101, 102”
From Update on the pathogenesis of atopic dermatitis. (2024) · cites this paper as [98]
The Discussion mentions filaggrin-related risk of atopic dermatitis and speculates about altered neonatal skin microbiota, but does not describe dysbiosis in patients with AD. Searches for reduced microbial diversity, S. aureus growth, skin pH, and antimicrobial deficiencies found no passage addressing those claims; the Experimental Procedures mention S. aureus only as a laboratory strain. Our copy provides section labels but no page numbers. (LLM, conf=0.76)
Experimental — accuracy not yet measuredColonization with skin commensal during the neonatal period is crucial for establishing immune tolerance through massive accumulation of active T regulatory cells in neonatal skin, collaboratively driven by hair follicle morphogenesis.
“colonization with skin commensal during the neonatal period is crucial for establishing immune tolerance through massive accumulation of active T regulatory cells in the neonatal skin, collaboratively driven by hair follicle morphogenesis.208,209”
From Interaction between microbiota and immunity in health and disease (2020) · cites this paper as [208]
Neonatal but not adult bacterial colonization attracts activated Tregs to skin and is necessary for induction of immune tolerance to skin commensals.
“neonatal, but not adult, bacterial colonization attracts activated regulatory T cells (Treg cells) to the skin and is necessary for the induction of immune tolerance to skin commensals171.”
From The microbiota of the respiratory tract: gatekeeper to respiratory health (2017) · cites this paper as [171]
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The gut microbiota promotes distal tissue regeneration via RORγ+ regulatory T cell emissaries
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Skin homeostasis: Mechanism and influencing factors
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- Authors
- Scharschmidt, T. C., Vasquez, K. S., Truong, H.-A., Gearty, S. V., Pauli, M. L., Nosbaum, A., Gratz, I. K., Otto, M., Moon, J. J., Liese, J., Abbas, A. K., Fischbach, M. A., & Rosenblum, M. D.
- Affiliations
- University of California, San Francisco (US)
- University of Salzburg (AT)
- National Institutes of Health (US)
- Harvard University (US)
- Universitätsklinikum Tübingen (DE)
- QB3 (US)
- Corresponding author
- Rosenblum, Michael D.
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2015-11
- Volume
- 43
- Issue
- 5
- Pages
- 1011-1021
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC4654993
- OpenAlex
- W2180997009
- Semantic Scholar
- 68e3547ebdf181f1414c5a4d59846f20d8195f8d
- Cited by
- 586
- References
- 58
- Citations by year
- 2026: 45 · 2025: 73 · 2024: 33 · 2023: 68 · 2022: 66 · 2021: 70 · 2020: 51 · 2019: 71 · 2018: 45 · 2017: 39 · 2016: 23 · 2015: 2
- FWCI
- 17.89
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Immunity (publishedVersion, cc-by-sa)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Dermatology Foundation
- National Institutes of Health (1dp2ar068130-01)
- University of California, San Francisco
- National Cancer Institute (P30CA082103)
- National Institute of Allergy and Infectious Diseases (R01AI107020, U19AI095261)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK063720, P30DK043351)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (DP2-AR068130, K08AR068409, R21AR066821, K08AR062064)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- regulatory T cells, neonatal skin, commensal bacteria, immune tolerance, Staphylococcus epidermidis, skin colonization, skin microbiome, adaptive immune response, Treg cell migration
- MeSH terms
- Animals, Animals, Newborn, Antigens, Bacterial, Immune Tolerance, Inflammation, Mice, Inbred C57BL, Molecular Sequence Data, Skin, Staphylococcal Infections, Staphylococcus epidermidis, T-Lymphocytes, Regulatory, Mice, Host-Pathogen Interactions, Microbiota
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