IL-17 is essential for host defense against cutaneous Staphylococcus aureus infection in mice
Open accessAbstract
Staphylococcus aureus is the most common cause of skin and soft tissue infections, and rapidly emerging antibiotic-resistant strains are creating a serious public health concern. If immune-based therapies are to be an alternative to antibiotics, greater understanding is needed of the protective immune response against S. aureus infection in the skin. Although neutrophil recruitment is required for immunity against S. aureus, a role for T cells has been suggested. Here, we used a mouse model of S. aureus cutaneous infection to investigate the contribution of T cells to host defense. We found that mice deficient in gammadelta but not alphabeta T cells had substantially larger skin lesions with higher bacterial counts and impaired neutrophil recruitment compared with WT mice. This neutrophil recruitment was dependent upon epidermal Vgamma5+ gammadelta T cell production of IL-17, but not IL-21 and IL-22. Furthermore, IL-17 induction required IL-1, TLR2, and IL-23 and was critical for host defense, since IL-17R-deficient mice had a phenotype similar to that of gammadelta T cell-deficient mice. Importantly, gammadelta T cell-deficient mice inoculated with S. aureus and treated with a single dose of recombinant IL-17 had lesion sizes and bacterial counts resembling those of WT mice, demonstrating that IL-17 could restore the impaired immunity in these mice. Our study defines what we believe to be a novel role for IL-17-producing epidermal gammadelta T cells in innate immunity against S. aureus cutaneous infection.
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IL-22-stimulated keratinocytes secrete increased amounts of defensins and other antimicrobial peptides that limit S. aureus proliferation.
“IL-22 stimulated keratinocytes, for example, secrete increased amounts of defensins and other antimicrobial peptides that limit S. aureus proliferation (Cho et al., 2010;Mulcahy et al., 2016).”
From Iron in infection and immunity (2020) · cites this paper as Cho et al., 2010
The Discussion says IL-17 and/or IL-22 may contribute to defense against cutaneous S. aureus infection through antimicrobial peptides, including β-defensins and cathelicidin. It does not establish that IL-22-stimulated keratinocytes secrete increased amounts of those peptides or that this secretion limits bacterial proliferation; the citing sentence presents a proposed mechanism as an observed fact. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIL-23 produced by keratinocytes can activate skin-resident IL-17+ γδT cells to control bacterial and fungal pathogen infections.
“it was previously reported that IL-23 produced by keratinocytes can activate skin-resident IL-17+ γδT cells to control bacterial and fungal pathogen infections.32,33”
From Skin-resident T cells play an important role in controlling skin colonization of Candidozyma (Candida) auris (2026) · cites this paper as [33]
The Results (page unavailable) show that IL-23 enhances IL-17 production by resident epidermal γδ T cells, and the Discussion (page unavailable) links these cells to defense against cutaneous S. aureus infection in mice. The paper does not establish that keratinocytes produce the IL-23 or that this pathway controls fungal infections. (LLM, conf=0.88)
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- Authors
- Cho, J. S., Pietras, E. M., Garcia, N. C., Ramos, R. I., Farzam, D. M., Monroe, H. R., Magorien, J. E., Blauvelt, A., Kolls, J. K., Cheung, A. L., Cheng, G., Modlin, R. L., & Miller, L. S.
- Affiliations
- University of California, Los Angeles (US)
- Portland VA Medical Center (US)
- Louisiana State University (US)
- Dartmouth College (US)
- Corresponding author
- Miller, Lloyd S.
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2010-05-03
- Volume
- 120
- Issue
- 5
- Pages
- 1762-1773
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC2860944
- OpenAlex
- W2092252407
- Cited by
- 658
- References
- 74
- Citations by year
- 2026: 22 · 2025: 28 · 2024: 33 · 2023: 30 · 2022: 32 · 2021: 44 · 2020: 47 · 2019: 53 · 2018: 42 · 2017: 41 · 2016: 59 · 2015: 48 · 2014: 38 · 2013: 44 · 2012: 36
- FWCI
- 19.21
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (7r01hl079142-05, AI047868, R24 CA92865)
- National Heart, Lung, and Blood Institute (R37HL079142, R01-HL079142)
- National Cancer Institute (R24CA092865, R24-CA92865)
- National Institute of Allergy and Infectious Diseases (R01AI078910, R37AI047868, R01AI056154, R01AI047868)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R03AR054534)
- California NanoSystems Institute
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Keywords
- IL-17, Staphylococcus aureus, skin infections, γδ T cells, neutrophil recruitment, innate immunity, interleukin-1, TLR2, IL-23, IL-17 receptor, skin and soft tissue infections, antibiotic resistance, immunotherapy
- MeSH terms
- Interleukin-22, Interleukin-21, Animals, Interferon-gamma, Interleukins, Male, Mice, Inbred C57BL, Models, Biological, Neutrophils, Skin, Staphylococcal Skin Infections, Staphylococcus aureus, Stem Cells, T-Lymphocytes, Interleukin-17, Mice
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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