The DOI matches its Crossref record; 63 of the 64 references it cites were found in a registry or an index.
Staphylococcus aureus Epicutaneous Exposure Drives Skin Inflammation via IL-36-Mediated T Cell Responses
Open accessAbstract
Staphylococcus aureus colonization contributes to skin inflammation in diseases such as atopic dermatitis, but the signaling pathways involved are unclear. Herein, epicutaneous S. aureus exposure to mouse skin promoted MyD88-dependent skin inflammation initiated by IL-36, but not IL-1α/β, IL-18, or IL-33. By contrast, an intradermal S. aureus challenge promoted MyD88-dependent host defense initiated by IL-1β rather than IL-36, suggesting that different IL-1 cytokines trigger MyD88 signaling depending on the anatomical depth of S. aureus cutaneous exposure. The bacterial virulence factor PSMα, but not α-toxin or δ-toxin, contributed to the skin inflammation, which was driven by IL-17-producing γδ and CD4+ T cells via direct IL-36R signaling in the T cells. Finally, adoptive transfer of IL-36R-expressing T cells to IL-36R-deficient mice was sufficient for mediating S. aureus-induced skin inflammation. Together, this study defines a previously unknown pathway by which S. aureus epicutaneous exposure promotes skin inflammation involving IL-36R/MyD88-dependent IL-17 T cell responses.
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“Interestingly, in a mouse model, colonization with S. aureus induces IL-36R- and IL-1R-dependent inflammation73.”
From Atopic dermatitis: an expanding therapeutic pipeline for a complex disease (2022) · cites this paper as [73]
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“there is increasing evidence that the IL-23–IL-17 axis as well as IL-36 (see above) may have a role, at least in some AD subtypes such as the so-called intrinsic form and in Asian patients73,103,117,123–125.”
From Atopic dermatitis: an expanding therapeutic pipeline for a complex disease (2022) · cites this paper as [73]
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Cites
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Community-associated meticillin-resistant Staphylococcus aureus
DeLeo, F. R., Otto, M. J., Kreiswirth, B. N., & Chambers, H. F. “. (2010) · The Lancet · doi:10.1016/s0140-6736(09)61999-1 · Cited by 1,534
Compartmentalized Control of Skin Immunity by Resident Commensals
Naik, S., Bouladoux, N., Wilhelm, C., Molloy, M. J., Salcedo, R., Kastenmuller, W., Deming, C., Quinones, M., Koo, L., Conlan, S., et al. (2012) · Science · doi:10.1126/science.1225152 · Cited by 1,092
Pivotal Role of Dermal IL-17-Producing γδ T Cells in Skin Inflammation
Cai, Y., Shen, X., Ding, C., Qi, C., Li, K., Li, X., Jala, V. R., Zhang, H., Wang, T., Zheng, J., et al. (2011) · Immunity · doi:10.1016/j.immuni.2011.08.001 · Cited by 1,049
A role for IL-25 and IL-33–driven type-2 innate lymphoid cells in atopic dermatitis
Salimi, M., Barlow, J. L., Saunders, S. P., Xue, L., Gutowska‐Owsiak, D., Wang, X., Huang, L.-C., Johnson, D., Scanlon, S. T., McKenzie, A. N. J., et al. (2013) · The Journal of Experimental Medicine · doi:10.1084/jem.20130351 · Cited by 1,012
Interleukin-36–Receptor Antagonist Deficiency and Generalized Pustular Psoriasis
Marrakchi, S., Guigue, P., Renshaw, B. R., Puel, A., Pei, X.-Y., Fraitag, S., Zribi, J., Bal, É., Cluzeau, C. V. M., Chrabieh, M., et al. (2011) · New England Journal of Medicine · doi:10.1056/nejmoa1013068 · Cited by 996
Gittler, J. K., Shemer, A., Suárez-Fariñas, M., Fuentes-Duculan, J., Gulewicz, K. J., Wang, C. Q. F., Mitsui, H., Cardinale, I., de Guzman Strong, C., Krueger, J. G., et al. (2012) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2012.07.012 · Cited by 981
Cited by
Sorted by citations
Pathogenicity and virulence of Staphylococcus aureus
Cheung, G. Y. C., Bae, J. S., & Otto, M. J. (2021) · Virulence · doi:10.1080/21505594.2021.1878688 · Cited by 1,554
IL-17 and IL-17-producing cells in protection versus pathology
Mills, K. H. G. (2022) · Nature reviews. Immunology · doi:10.1038/s41577-022-00746-9 · Cited by 1,068
Skin microbiota–host interactions
Chen, Y. E., Fischbach, M. A., & Belkaid, Y. (2018) · Nature · doi:10.1038/nature25177 · Cited by 815
Atopic dermatitis: an expanding therapeutic pipeline for a complex disease
Bieber, T. (2022) · Nature Reviews Drug Discovery · doi:10.1038/s41573-021-00266-6 · Cited by 623
Molecular Mechanisms of Atopic Dermatitis Pathogenesis
Sroka-Tomaszewska, J., & Trzeciak, M. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22084130 · Cited by 605
Metadata
- Authors
- Liu, H., Archer, N. K., Dillen, C. A., Wang, Y., Ashbaugh, A. G., Ortines, R. V., Kao, T., Lee, S. K., Cai, S. S., Miller, R. J., Marchitto, M. C., Zhang, E., Riggins, D. P., Plaut, R. D., Stibitz, S., Geha, R. S., & Miller, L. S.
- Affiliations
- Johns Hopkins University (US)
- Center for Biologics Evaluation and Research (US)
- Boston Children's Hospital (US)
- Corresponding author
- Miller, Lloyd S.
- ORCID
- Venue
- Cell Host & Microbe
- Publisher
- Elsevier BV
- Published
- 2017-11
- Volume
- 22
- Issue
- 5
- Pages
- 653-666.e5
- ISSN
- 1931-3128 (ISSN-L)
- PMC
- PMC5774218
- OpenAlex
- W2767217104
- Cited by
- 263
- References
- 64
- Citations by year
- 2026: 26 · 2025: 27 · 2024: 41 · 2023: 33 · 2022: 30 · 2021: 29 · 2020: 27 · 2019: 31 · 2018: 16 · 2017: 3
- FWCI
- 23.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Host & Microbe (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (UM2AI117870)
- NIH (R01AR069502)
- Pfizer (WI214880)
- Topics
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Health Sciences › Medicine › Infectious Diseases › Antimicrobial Resistance in Staphylococcus
- Keywords
- Staphylococcus aureus, skin inflammation, IL-36, IL-36 receptor, MyD88 signaling, IL-17, γδ T cells, CD4+ T cells, staphylococcal virulence factors, atopic dermatitis, IL-1β, intradermal challenge, adoptive transfer
- MeSH terms
- Interleukin-33, Animals, Bacterial Toxins, Dermatitis, Atopic, Disease Models, Animal, Female, Hemolysin Proteins, Host-Parasite Interactions, Inflammation, Interleukin-1, Male, Mice, Inbred BALB C, Skin, Staphylococcal Infections, Staphylococcus aureus, T-Lymphocytes, CD4-Positive T-Lymphocytes, Cytokines, Receptors, Interleukin-1, Interleukin-17, Interleukin-18, Virulence Factors, Mice, Interleukin-1alpha, Interleukin-1beta, Myeloid Differentiation Factor 88
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