The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
IL-23 and IL-17A, but Not IL-12 and IL-22, Are Required for Optimal Skin Host Defense against Candida albicans
Open accessAbstract
IL-23 and Th17 cells play important roles in host defense against systemic infections with extracellular bacteria and fungi, although their roles in immunity against localized skin infections are less well defined. Here, the contributions of IL-23 and Th17 cytokines in host defense against cutaneous Candida albicans infection were evaluated. Mice deficient in IL-23 or IL-17A demonstrated delayed healing and decreased IL-17A production after skin infection with C. albicans compared with wild-type mice or mice deficient in IL-12 or IL-22. Histologic examination revealed epidermal hyperplasia overlying infected dermis four days postinoculation in wild-type mice. In IL-23–deficient mice, fungal burden was greater in skin, neither IL-17A nor IL-22 mRNAs were expressed postinfection, and these mice demonstrated only minimal epidermal hyperplasia. Exogenous recombinant IL-17A injected at the site of skin infection promoted more rapid healing of candidiasis in both wild-type mice and mice deficient in IL-23 and IL-12. Taken together, these results demonstrate that IL-23 and IL-17A, but not IL-12 and IL-22, are required for optimal host defense against cutaneous candidiasis. In addition, recombinant IL-17A may serve as a potential therapy to enhance healing in individuals with chronic cutaneous candidiasis.
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“However, compared to C. albicans-infected mice, C. auris skin infection induces a significantly decreased number of IL-17- and IL-22-producing TCRβ+ cells that are important for host defense against fungal pathogens.”
From Differential skin immune responses in mice intradermally infected with Candida auris and Candida albicans (2023) · cites this paper as [18]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“T cells such as TCRβ+ IL-17+ T cells are critical for host defense against Candida pathogens, including those in the skin (10, 18).”
From Differential skin immune responses in mice intradermally infected with Candida auris and Candida albicans (2023) · cites this paper as [18]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“These findings suggest that IL-17-mediated immune responses are critical for protection against C. auris and C. albicans skin infection (4, 18, 25).”
From Differential skin immune responses in mice intradermally infected with Candida auris and Candida albicans (2023) · cites this paper as [18]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Furthermore, previous findings suggest that Th17 cells are required for cutaneous host defense, while Th1 response is critical against systemic C. albicans infection (18, 25).”
From Differential skin immune responses in mice intradermally infected with Candida auris and Candida albicans (2023) · cites this paper as [18]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“the IL-17 pathway, which plays a critical role in antifungal host defense, including C. auris [4, 39]”
From Single-cell transcriptomics unveils skin cell specific antifungal immune responses and IL-1Ra- IL-1R immune evasion strategies of emerging fungal pathogen Candida auris (2024) · cites this paper as [39]
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Citations
Cites
Interleukin-22, a TH17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis
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“This is a somewhat surprising finding given that injections of recombinant IL-23 into murine skin induced epidermal hyperplasia in WT mice but failed to do so in mice deficient in IL-22 (26).”
Leonardi, C. L., Kimball, A. B., Papp, K. A., Yeilding, N. M., Guzzo, C. A., Wang, Y., Li, S., Dooley, L. T., & Gordon, K. B. (2008) · The Lancet · doi:10.1016/s0140-6736(08)60725-4 · Cited by 1,870
Interleukin-17 and Type 17 Helper T Cells
Miossec, P., Korn, T., & Kuchroo, V. K. (2009) · New England Journal of Medicine · doi:10.1056/nejmra0707449 · Cited by 1,409 · cited 1×
“Th17 cells produce cytokines, principally IL-17A and IL-22, which mediate protection from infection at mucocutaneous surfaces (18, 19).”
Papp, K. A., Langley, R. G. B., Lebwohl, M., Krueger, G. G., Szapary, P. O., Yeilding, N. M., Guzzo, C. A., Hsu, M.-C., Wang, Y., Li, S., et al. (2008) · The Lancet · doi:10.1016/s0140-6736(08)60726-6 · Cited by 1,358
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Impaired TH17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome
Milner, J. D., Brenchley, J. M., Laurence, A., Freeman, A. F., Hill, B. J., Elias, K. M., Kanno, Y., Spalding, C., Elloumi, H. Z., Paulson, M. L., et al. (2008) · Nature · doi:10.1038/nature06764 · Cited by 1,157
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“Through material transfer agreements, IL17A2/2 mice were obtained from Dr. Yoichiro Iwakura (Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Japan) (25), and IL-222/2 mice and IL-23p192/2 mice were obtained from Dr. Wenjun Ouyang and Dr. Frederic de Sauvage (Genentech, South San Fr…”
Conti, H. R., Shen, F., Nayyar, N., Stocum, E., Sun, J. N., Lindemann, M. J., Ho, A. W., Hai, J. H., Yu, J. J., Jung, J. W., et al. (2009) · Journal of Experimental Medicine · doi:10.1084/jem.20081463 · Cited by 1,024 · cited 2×
“In addition, another study using a mouse model of oral candidiasis demonstrated that mice deficient in Th17 cells developed more severe disease than Th1 cell-deficient mice (17).”
Requirement of Interleukin‐17A for Systemic Anti– Candida albicans Host Defense in Mice
Huang, W., Na, L., Fidel, P. L., & Schwarzenberger, P. (2004) · The Journal of Infectious Diseases · doi:10.1086/422329 · Cited by 859 · cited 1×
“IL-17AR–deficient mice had reduced survival rates after systemic Candida challenge (36).”
Hyper-IgE Syndrome with Recurrent Infections — An Autosomal Dominant Multisystem Disorder
Grimbacher, B., Holland, S. M., Gallin, J. I., Greenberg, F., Hill, S. C., Malech, H. L., Miller, J., O’Connell, A. C., & Puck, J. M. (1999) · New England Journal of Medicine · doi:10.1056/nejm199903043400904 · Cited by 801 · cited 3×
“albicans in patients who suffer from Job’s syndrome, chronic mucocutaneous candidiasis, and HIV/AIDS (2, 23, 24, 28).”
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Aono, Y., Amano, T., Matsudo, H., Hirose, S., Morishige, T., Kikuta, N., Okada, H., & Hamaura, N. (2016) · Folia Pharmacologica Japonica · doi:10.1254/fpj.148.205
Candida and host cell interactions associated with colonisation and infection
Rogers, H. (2017) · ORCA Online Research @Cardiff (Cardiff University)
Candida albicans adaption to host microenvironments drives immune evasion
Lopes, J. P. (2018) · KTH Publication Database DiVA (KTH Royal Institute of Technology)
Elucidating Role of Bacteria in Psoriatic Disease: From Skin and Gut PerspectivesPreprint
Yermekbayeva, B., Algazina, T., Razbekova, M., Pinhasov, A., Batpenova, G., & Kushugulova, A. R. (2018) · Preprints.org · doi:10.20944/preprints201809.0215.v1
“[27] Kagami S, Rizzo HL, Kurtz SE, Miller LS, Blauvelt A.”
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The Oral Mucosa-Fungi Interactome
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INTERLEUKIN-17-MEDIATED ADAPTIVE IMMUNITY TO CANDIDA ALBICANS IN OROPHARYNGEAL CANDIDIASIS
Hernández‐Santos, N. (2012) · D-Scholarship@Pitt (University of Pittsburgh)
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Tamargo, M. G. D. A. (2011) · theses.fr (ABES) · doi:10.70675/8febaec4z61f1z41f7z9621zf9a3ffc15ed7
IL - 17 et réponse inflammatoire systémique : focus sur le foie et le muscle
Beringer, A. (2018) · theses.fr (ABES) · doi:10.70675/2d9a348ez5879z4d92z938fz1e4047d398bc
Li, M., Ni, J., Zhang, L., Chen, C., Ye, J., & Chen, N. (2026) · Expert Opinion on Drug Safety · doi:10.1080/14740338.2026.2701664
Metadata
- Authors
- Kagami, S., Rizzo, H. L., Kurtz, S. E., Miller, L. S., & Blauvelt, A.
- Affiliations
- Oregon Health & Science University (US)
- Portland VA Medical Center (US)
- University of California, Los Angeles (US)
- Corresponding author
- Kagami, Shinji
- Blauvelt, Andrew
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-11-01
- Volume
- 185
- Issue
- 9
- Pages
- 5453-5462
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC3076054
- OpenAlex
- W2170016098
- Cited by
- 216
- References
- 42
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 8 · 2023: 5 · 2022: 11 · 2021: 7 · 2020: 9 · 2019: 9 · 2018: 11 · 2017: 21 · 2016: 17 · 2015: 29 · 2014: 25 · 2013: 10 · 2012: 19
- FWCI
- 7.29
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Veterans Affairs
- Naito Foundation
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases (R01AI078910)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R21AR054495)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Keywords
- IL-23, IL-17A, IL-12, IL-22, Th17 cells, cutaneous candidiasis, Candida albicans, epidermal hyperplasia, fungal burden
- MeSH terms
- Interleukin-22, Animals, Candida albicans, Candidiasis, Cutaneous, Enzyme-Linked Immunosorbent Assay, Immunohistochemistry, Interleukins, Mice, Inbred C57BL, Skin, Mice, Knockout, Interleukin-12, Reverse Transcriptase Polymerase Chain Reaction, Interleukin-17, Mice, Interleukin-23
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