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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]
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“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]
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“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]
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“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]
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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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“Reminiscent of what is known from other experimental models of fungal infection in mice (Conti et al., 2014; Gladiator et al., 2013; Hernández-Santos et al., 2018; Kagami et al., 2010; Kashem et al., 2015; Sparber et al., 2018), the initial peak of IL-17 expression by innate immune cells, in particular gd T cells, app…”
BackgroundOral-resident natural Th17 cells and γδ T cells control opportunistic Candida albicans infections
Conti, H. R., Peterson, A. C., Brane, L., Huppler, A. R., Hernández-Santos, N., Whibley, N., Garg, A. V., Simpson-Abelson, M. R., Gibson, G. A., Mamo, A. J., et al. (2014) · Journal of Experimental Medicine · doi:10.1084/jem.20130877 · Cited by 254
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Hernández‐Santos, N., Huppler, A. R., Peterson, A. C., Khader, S. A., McKenna, K. C., & Gaffen, S. L. (2012) · Mucosal Immunology · doi:10.1038/mi.2012.128 · Cited by 197
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“albicans [23,56,57], and pulmonary infection with H.”
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Candida albicans and Candida glabrata : global priority pathogens
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BackgroundMannan induces ROS-regulated, IL-17A–dependent psoriasis arthritis-like disease in mice
Khmaladze, I., Kelkka, T., Guérard, S., Wing, K., Pizzolla, A., Saxena, A., Lundqvist, K., Holmdahl, M., Nandakumar, K. S., & Holmdahl, R. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1405798111 · Cited by 156
“Clearly, an immune response to yeast is dependent on Th17 (IL-23/IL-17A) pathway (24).”
BackgroundSkin Immunity to Candida albicans
Kashem, S. W., & Kaplan, D. H. (2016) · Trends in Immunology · doi:10.1016/j.it.2016.04.007 · Cited by 152
“albicans due to decreased IL-17, as well as reduced neutrophil infiltrates and epithelial hyperplasia [13,14,67,68].”
BackgroundMucocutaneous IL-17 immunity in mice and humans: host defense vs. excessive inflammation
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“albicans than wild-type mice.(44) Mice lacking IL-12p40 or IL23p19, the two subunits of IL-23, which is essential for TH17 cell development and maintenance in mice,(45) also have high fungal burdens in the skin when challenged with C.”
Mucocutaneous candidiasis: the IL-17 pathway and implications for targeted immunotherapy
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“Similarly, immunity to dermal and disseminated candidiasis in mice is regulated by the IL-17 pathway [18,19].”
BackgroundMucosal Immunity and Candida albicans Infection
Moyes, D. L., & Naglik, J. R. (2011) · Clinical and Developmental Immunology · doi:10.1155/2011/346307 · Cited by 156
“…infection of peripheral blood mononuclear cells by live C. albicans results in inhibition of IL-17 secretion resulting from the effects of C. albicans-released 5-hydroxytryptophan metabolites [70] with a concurrent suppression of immunity to the fungus, suggesting that IL-17 may be…”
BackgroundField, K. A., Johnson, J. S., Lilley, T. M., Reeder, S. M., Rogers, E. J., Behr, M. J., & Reeder, D. M. (2015) · PLoS Pathogens · doi:10.1371/journal.ppat.1005168 · Cited by 144
“These T cell responses can be mediated by Th17 cells [32, 33] or, in some cases, Th1 cells [34], with Th2 responses typically associated with greater susceptibility [35].”
BackgroundA Double Edged Sword Role of Interleukin-22 in Wound Healing and Tissue Regeneration
Arshad, T., Mansur, F., Pálek, R., Manzoor, S., & Liška, V. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.02148 · Cited by 138
“In addition, IL22 exhibit mild role in protecting against cutaneous candidiasis in mice (98).”
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“In models of oral infection (8) and skin infection (18) with C.”
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BackgroundInfluentialSafety of secukinumab in the treatment of psoriasis
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“Individuals with these diseases are susceptible to mucocutaneous candidiasis [18]; similarly, IL-17A knockout mice are prone to chronic cutaneous candidiasis [19].”
BackgroundSelf-citationIL-17 signaling in host defense against Candida albicans
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“Similar results were found in studies of skin candidiasis in mice (30).”
ResultOral epithelial IL-22/STAT3 signaling licenses IL-17-mediated immunity to oral mucosal candidiasis
Aggor, F. E. Y., Break, T. J., Trevejo-Nuñez, G., Whibley, N., Coleman, B. M., Bailey, R. D., Kaplan, D. H., Naglik, J. R., Shan, W., Shetty, A. C., et al. (2020) · Science Immunology · doi:10.1126/sciimmunol.aba0570 · Cited by 119
Adaptive Immunity to FungiPreprint
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“In models of dermal and oral infection, IL-23deficient animals develop progressively worse disease (Conti et al. 2009; Kagami et al. 2010).”
Valdez, P. A., Vithayathil, P. J., Janelsins, B., Shaffer, A. L., Williamson, P. R., & Datta, S. K. (2012) · Immunity · doi:10.1016/j.immuni.2012.02.013 · Cited by 118
“The role of IL-22 and the potential effect of its enhancement by PGE2 in fungal infections is less clear, with evidence that it may contribute to immunity in some contexts (Burbelo et al., 2010; Kisand et al., 2010; Puel et al., 2010; Zelante et al., 2011) but not in others (Kagami et al., 2010).”
The Biology and Functions of Th22 Cells
Jia, L., & Wu, C. Y. (2014) · Advances in experimental medicine and biology · doi:10.1007/978-94-017-9487-9_8 · Cited by 125
Role of Th17 and IL-17 Cytokines on Inflammatory and Auto-immune Diseases
Akhter, S., Tasnim, F. M., Islam, M. N., Rauf, A., Mitra, S., Emran, T. B., Alhumaydhi, F. A., Khalil, A. A., Aljohani, A. S. M., Abdulmonem, W. A., et al. (2023) · Current Pharmaceutical Design · doi:10.2174/1381612829666230904150808 · Cited by 125
IL-17-mediated antifungal defense in the oral mucosa is independent of neutrophils
Trautwein-Weidner, K., Gladiator, A., Nur, S., Diethelm, P., & LeibundGut‐Landmann, S. (2014) · Mucosal Immunology · doi:10.1038/mi.2014.57 · Cited by 114
“albicans on IL-17 signaling.(9,10) The family of IL-17 cytokines consists of six members (IL-17A–IL-17F).”
BackgroundChiricozzi, A., Suárez‐Fariñas, M., Fuentes‐Duculan, J., Cueto, I., Li, K., Tian, S., Brodmerkel, C. M., & Krueger, J. G. (2015) · British Journal of Dermatology · doi:10.1111/bjd.14034 · Cited by 108
Astry, B., Venkatesha, S. H., & Moudgil, K. D. (2015) · Cytokine · doi:10.1016/j.cyto.2014.11.020 · Cited by 109
The Th17 axis in psoriatic disease: pathogenetic and therapeutic implications
Marinoni, B., Ceribelli, A., Massarotti, M. S., & Selmi, C. F. (2014) · Autoimmunity Highlights · doi:10.1007/s13317-013-0057-4 · Cited by 105
“corticosteroid therapies or drugs targeting the IL23/Th17/ IL17 pathway [52].”
BackgroundInnate Defense against Fungal PathogensPreprint
Drummond, R. A., Gaffen, S. L., Hise, A. G., & Brown, G. D. (2014) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a019620 · Cited by 102
“For example, in dermal Candida infections, the gdT cell population was shown to be the dominant source of IL-17, which contributed to the resolution of skin lesions (Kagami et al. 2010; Hirota et al. 2011; Igyarto et al. 2011).”
Dühring, S., Germerodt, S., Skerka, C., Zipfel, P. F., Dandekar, T., & Schuster, S. (2015) · Frontiers in Microbiology · doi:10.3389/fmicb.2015.00625 · Cited by 108
The Gut-Liver Axis in Cholestatic Liver Diseases
Blesl, A., & Stadlbauer, V. (2021) · Nutrients · doi:10.3390/nu13031018 · Cited by 102
IL-17 and IL-17-producing cells and liver diseases, with focus on autoimmune liver diseases
Beringer, A., & Miossec, P. (2018) · Autoimmunity Reviews · doi:10.1016/j.autrev.2018.06.008 · Cited by 96
Fungi as Part of the Microbiota and Interactions with Intestinal Bacteria
Kapitan, M., Niemiec, M. J., Steimle, A., Frick, J.-S., & Jacobsen, I. D. (2018) · Current topics in microbiology and immunology · doi:10.1007/82_2018_117 · Cited by 101
Opportunistic yeast pathogens: reservoirs, virulence mechanisms, and therapeutic strategies
Polvi, E. J., Li, X., O’Meara, T. R., Leach, M. D., & Cowen, L. E. (2015) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-015-1860-z · Cited by 94
“albicans infection [328], suggesting that both IL-17A and IL-17F are required for the defense against”
BackgroundSyk Signaling in Dendritic Cells Orchestrates Innate Resistance to Systemic Fungal Infection
Whitney, P. G., Bär, E., Osorio, F., Rogers, N. C., Schraml, B. U., Deddouche, S., LeibundGut‐Landmann, S., & Sousa, C. R. E. (2014) · PLoS Pathogens · doi:10.1371/journal.ppat.1004276 · Cited by 94
“In addition, IL-23p19 is important for early resistance to candidiasis [55,56] and can be synthesized by DCs in a Syk-dependent manner upon stimulation with CLR agonists [27].”
BackgroundRole of IL-22 in Microbial Host Defense
Eidenschenk, C., Rutz, S., Liesenfeld, O., & Ouyang, W. (2014) · Current topics in microbiology and immunology · doi:10.1007/978-3-662-43492-5_10 · Cited by 93
Tailored Immune Responses: Novel Effector Helper T Cell Subsets in Protective Immunity
Kara, E. E., Comerford, I., Fenix, K. A., Bastow, C. R., Whyte, C. E., McKenzie, D. R., & McColl, S. R. (2014) · PLoS Pathogens · doi:10.1371/journal.ppat.1003905 · Cited by 87
“Critical requirements for the IL-23/IL-17 axis in protective immunity have also been described in murine models of dermal candidiasis [98].”
BackgroundMicrobial-Induced Th17: Superhero or Supervillain?
McGeachy, M. J., & McSorley, S. J. (2012) · The Journal of Immunology · doi:10.4049/jimmunol.1201834 · Cited by 76
“In contrast, neither IL-17F nor IL-22 is essential for host resistance to Candida infection (83, 84, 86).”
BackgroundKim, J.-Y., Park, M., Kim, Y., Ryu, K., Lee, K. H., Cho, K., & Woo, S. (2017) · Journal of Tissue Engineering and Regenerative Medicine · doi:10.1002/term.2423 · Cited by 73
“The initial activation of dendritic cells by cutaneous pathogens leads to secretion of interleukin (IL)-23, which promotes Th17 differentiation (Kagami et al., 2010; Piskin et al., 2006).”
BackgroundHuman IL-23 is essential for IFN-γ–dependent immunity to mycobacteria
Philippot, Q., Ogishi, M., Bohlen, J., Puchan, J., Arias, A. A., Nguyen, T., Martín-Fernández, M., Conil, C., Rinchai, D., Momenilandi, M., et al. (2023) · Science Immunology · doi:10.1126/sciimmunol.abq5204 · Cited by 72
Maher, B. M., Mulcahy, M. E., Murphy, A. G., Wilk, M. M., O’Keeffe, K. M., Geoghegan, J. A., Lavelle, E. C., & McLoughlin, R. M. (2013) · Infection and Immunity · doi:10.1128/iai.01026-13 · Cited by 73
“Mice deficient in IL-17 are highly susceptible to a number of bacterial and fungal infections, including Klebsiella pneumoniae (6), Escherichia coli (7), and Candida albicans (8).”
BackgroundLangley, R. G. B., Papp, K. A., Gottlieb, A. B., Krueger, G. G., Gordon, K. B., Williams, D., Valdes, J. M., Setze, C. M., & Strober, B. E. (2012) · Journal of the European Academy of Dermatology and Venereology · doi:10.1111/j.1468-3083.2012.04705.x · Cited by 70
Striking a balance: fungal commensalism versus pathogenesis
Iliev, I. D., & Underhill, D. M. (2013) · Current Opinion in Microbiology · doi:10.1016/j.mib.2013.05.004 · Cited by 71
“However, IL-22 appears to not play a role in host defense against Candida skin infection in mice [35].”
BackgroundNew insight into the pathogenesis of nail psoriasis and overview of treatment strategies
Ventura, A., Mazzeo, M., Gaziano, R., Galluzzo, M., Bianchi, L., & Campione, E. (2017) · Drug Design Development and Therapy · doi:10.2147/dddt.s136986 · Cited by 68
“33 Candida can stimulate the production of superantigens, determining non-specific T-cell activation and secretion of cytokines that can initiate the psoriatic process.”
Antibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis
Whibley, N., Tritto, E., Traggiai, E., Kolbinger, F., Moulin, P., Brees, D., Coleman, B. M., Mamo, A. J., Garg, A. V., Jaycox, J. R., et al. (2016) · Journal of Leukocyte Biology · doi:10.1189/jlb.4a0915-428r · Cited by 67
The intestinal microbiota and microenvironment in liver
Ma, H.-D., Wang, Y., Chang, C. C.-C., Gershwin, M. E., & Lian, Z. (2014) · Autoimmunity Reviews · doi:10.1016/j.autrev.2014.10.013 · Cited by 64
“important role in defense against extracellular bacteria and fungi [108, 109], particularly at epithelial and mucosal surfaces [110].”
BackgroundIL-17C is required for lethal inflammation during systemic fungal infection
Huang, J., Meng, S., Hong, S., Lin, X., Jin, W., & Dong, C. (2016) · Cellular & Molecular Immunology · doi:10.1038/cmi.2015.56 · Cited by 61
Cytokines and the regulation of fungus-specific CD4 T cell differentiation
Espinosa, V., & Rivera, A. (2011) · Cytokine · doi:10.1016/j.cyto.2011.11.005 · Cited by 64
“Mice deficient in IL-17A, IL17RA or treated with neutralizing antibodies display enhanced fungal burden and susceptibility to Candida, Blastomyces and Histoplasma [18,25,28,29, 95,106].”
InfluentialEmerging IL-12 family cytokines in the fight against fungal infections
Thompson, A., & Orr, S. J. (2018) · Cytokine · doi:10.1016/j.cyto.2018.05.019 · Cited by 61
Tissue-resident memory Th17 cells maintain stable fungal commensalism in the oral mucosa
Kirchner, F. R., & LeibundGut-Landmann, S. (2021) · Mucosal Immunology · doi:10.1038/s41385-020-0327-1 · Cited by 59
Conti, H. R., Whibley, N., Coleman, B. M., Garg, A. V., Jaycox, J. R., & Gaffen, S. L. (2015) · PLoS ONE · doi:10.1371/journal.pone.0122807 · Cited by 61
“It is striking, however, that no patients with CMC have yet emerged with defects in the IL-17C/IL-17RE pathway, whereas an ever-increasing number have been found that PLOS ONE | DOI:10.1371/journal.pone.0122807 April 7, 2015 10 / 14 are impaired in the IL-17A/F-IL-17RA pathway [4].”
BackgroundMethodResultInfluentialBeyond Candida albicans: Mechanisms of immunity to non-albicans Candida species
Whibley, N., & Gaffen, S. L. (2015) · Cytokine · doi:10.1016/j.cyto.2015.07.025 · Cited by 62
Brothers in Arms: Th17 and Treg Responses in Candida albicans Immunity
Whibley, N., & Gaffen, S. L. (2014) · PLoS Pathogens · doi:10.1371/journal.ppat.1004456 · Cited by 58
“Similarly, IL-23 and IL-17A mice display susceptibility to dermal candidiasis [8].”
BackgroundThe NLRP 3 inflammasome contributes to host protection during Sporothrix schenckii infection
Gonçalves, A. C., Ferreira, L. S., Manente, F. A., de Faria, C. M. Q. G., Polesi, M. C., de Andrade, C. R., Zamboni, D. S., & Carlos, I. Z. (2017) · Immunology · doi:10.1111/imm.12719 · Cited by 55
The role of pattern recognition receptors in the innate recognition of Candida albicans
Zheng, N.-X., Wang, Y., Hu, D.-D., Yan, L., & Jiang, Y.-Y. (2015) · Virulence · doi:10.1080/21505594.2015.1014270 · Cited by 52
“albicans at the majority of mucosal sites in the body.(165,166) The importance of Th17 cells in anti-Candida responses is not only portrayed by data from mice models, but also from human patients.”
BackgroundCytokine-Based Therapy in Psoriasis
Mitra, A., Fallen, R. S., & Lima, H. (2012) · Clinical Reviews in Allergy & Immunology · doi:10.1007/s12016-012-8306-2 · Cited by 55
“development [30].”
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A Clinician’s Guide to the Diagnosis and Treatment of Candidiasis in Patients with Psoriasis
Armstrong, A. W., Bukhalo, M., & Blauvelt, A. (2016) · American Journal of Clinical Dermatology · doi:10.1007/s40257-016-0206-4 · Cited by 56
Self-citationLing, Y., & Puel, A. (2014) · Actas Dermo-Sifiliográficas · doi:10.1016/s0001-7310(14)70016-x · Cited by 54
Nakada, T., Russell, J. A., Boyd, J. H., & Walley, K. R. (2011) · Critical Care · doi:10.1186/cc10515 · Cited by 54
“In contrast, deficiency of the IL17 response impairs bacterial clearance, delays recovery from infection [1,11] and increases susceptibility to infection [12-15].”
BackgroundT helper type 17 in psoriasis: From basic immunology to clinical practice
Chiu, H., Cheng, Y., & Tsai, T. (2012) · Dermatologica Sinica · doi:10.1016/j.dsi.2012.08.002 · Cited by 54
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Innate Lymphocytes in Psoriasis
Polese, B., Zhang, H., Thurairajah, B., & King, I. L. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.00242 · Cited by 54
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Maher, C. O., Dunne, K., Comerford, R., O’Dea, S., Loy, A., Woo, J., Rogers, T. R., Mulcahy, F. M., Dunne, P. J., & Doherty, D. G. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1403066 · Cited by 50
“albicans infections are common in humans with inherited deficiencies of the IL-17 pathway (such as IL-17 deficiency or mutations in the IL-17R or STAT1) (14, 15) and in knockout mice that lack IL-17 or IL-23 (6, 16).”
BackgroundTh1 and Th17 Immune Responses Act Complementarily to Optimally Control Superficial Dermatophytosis
Heinen, M.-P., Cambier, L., Antoine, N., Gabriel, A., Gillet, L., Bureau, F., & Mignon, B. R. (2018) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2018.07.040 · Cited by 50
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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