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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IL-17- and IL-22-producing TCRβ+ cells are important for host defense against fungal pathogens.
“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 <i>Candida auris</i> and <i>Candida albicans</i> (2023) · cites this paper as [18]
The Discussion reports that IL-17A is important for defense against cutaneous C. albicans, and that CD3+ T cells produce it. But it says IL-22 is not required in this model: IL-22-deficient mice had neither delayed healing nor increased fungal burdens. The paper does not establish the claimed importance of IL-17- and IL-22-producing TCRβ+ cells specifically. (LLM, conf=0.88)
Experimental — accuracy not yet measuredT cells such as TCRβ+ IL-17+ T cells are critical for host defense against Candida pathogens, including those in the skin.
“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 <i>Candida auris</i> and <i>Candida albicans</i> (2023) · cites this paper as [18]
The Results (page unavailable) identify CD3+ T cells as the main IL-17A-producing cells in infected mouse skin, and the Abstract reports that IL-17A is required for optimal defense against cutaneous Candida albicans. The paper does not identify those cells as TCRβ+ or establish that this specific T-cell subset is critical; its findings also concern C. albicans rather than Candida pathogens generally. (LLM, conf=0.85)
Experimental — accuracy not yet measuredIL-17-mediated immune responses are critical for protection against C. auris and C. albicans skin infection.
“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 <i>Candida auris</i> and <i>Candida albicans</i> (2023) · cites this paper as [18]
The Discussion states that IL-17A is essential for host defense against cutaneous C. albicans infection. The paper studies C. albicans in mice, not C. auris, so it does not support the C. auris part of the sentence. (LLM, conf=0.88)
Experimental — accuracy not yet measuredTh17 cells are required for cutaneous host defense, while Th1 response is critical against systemic C. albicans infection.
“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 <i>Candida auris</i> and <i>Candida albicans</i> (2023) · cites this paper as [18]
The Abstract reports that IL-23 and IL-17A are required for optimal defense against cutaneous C. albicans infection, and says Th1 responses are believed to be critical against C. albicans infection generally. It does not establish that Th17 cells themselves are required in skin or specifically that Th1 responses are critical against systemic infection; the Discussion notes that other cells may produce IL-17A. Page numbers are unavailable in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe IL-17 pathway plays a critical role in antifungal host defense, including C. auris.
“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]
The Discussion (page unavailable) reports that IL-17A is a key mediator of skin defense against C. albicans in mice. The paper does not address C. auris, so it does not support extending that finding to this species. (LLM, conf=0.90)
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Self-citationRecent advances in the IL-17 cytokine family
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The Cytokine IL-22 Promotes Pathogen Colonization by Suppressing Related Commensal Bacteria
Behnsen, J., Jellbauer, S., Wong, C. P., Edwards, R. A., George, M. D., Ouyang, W., & Raffatellu, M. (2014) · Immunity · doi:10.1016/j.immuni.2014.01.003 · Cited by 279 · see citing works
“…defenses, many pathogens colonize mucosal surfaces and establish an infection; for example, IL-22 failed to reduce oral infection with Candida albicans and genital infection with Neisseria gonorrhoeae (Feinen and Russell, 2012; Kagami et al., 2010), although the basis for this was not investigated.”
InfluentialPapp, K. A., Thaçi, D., Reich, K., Riedl, E., Langley, R. G. B., Krueger, J. G., Gottlieb, A. B., Nakagawa, H., Bowman, E. P., Mehta, A., et al. (2015) · British Journal of Dermatology · doi:10.1111/bjd.13932 · Cited by 276 · see citing works
Cutting Edge: Identification of a Motile IL-17–Producing γδ T Cell Population in the Dermis
Gray, E. E., Suzuki, K., & Cyster, J. G. (2011) · The Journal of Immunology · doi:10.4049/jimmunol.1100427 · Cited by 263 · see citing works
“In summary, although several studies have identified a critical role for IL-17 in the protective response mounted in the early hours to days of cutaneous infections (4, 5, 12), the precise cellular source of this IL-17 was not defined (5, 12) or was suggested to be DETCs (4).”
Sparber, F., De Gregorio, C., Steckholzer, S., Ferreira, F. M., Dolowschiak, T., Ruchti, F., Kirchner, F. R., Mertens, S., Prinz, I., Joller, N., et al. (2019) · Cell Host & Microbe · doi:10.1016/j.chom.2019.02.002 · Cited by 255 · see citing works
“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…”
BackgroundConti, 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 · see citing works
The role of interleukin-17 in tumor development and progression
Zhao, J., Chen, X., Herjan, T., & Li, X. (2019) · The Journal of Experimental Medicine · doi:10.1084/jem.20190297 · Cited by 253 · see citing works
Wüthrich, M., Deepe, G. S., & Klein, B. S. (2012) · Annual Review of Immunology · doi:10.1146/annurev-immunol-020711-074958 · Cited by 225 · see citing works
“In models of dermal and oral infection, IL-23deficient animals develop progressively worse disease (Conti et al. 2009; Kagami et al. 2010).”
Zhong, B., Liu, X., Wang, X., Chang, S. H., Liu, X., Wang, A., Reynolds, J. M., & Dong, C. (2012) · Nature Immunology · doi:10.1038/ni.2427 · Cited by 206 · see citing works
Adaptive immune responses to Candida albicans infection
Richardson, J. P., & Moyes, D. L. (2015) · Virulence · doi:10.1080/21505594.2015.1004977 · Cited by 206 · see citing works
“albicans at these locations.(33,34) Interestingly, IL-17 and IL-22 do not contribute to immune protection in vaginal mucosa,(35) highlighting the subtle differences in immune response requirements at different mucosal sites.”
BackgroundThe human gut mycobiome: pitfalls and potentials—a mycologist’s perspective
Haute, M. J. S. V., & Hallen‐Adams, H. E. (2015) · Mycologia · doi:10.3852/15-147 · Cited by 197 · see citing works
“Mice deficient in components of the IL-17 pathway have increased susceptibility to oral candidiasis and skin infections (Conti et al. 2009, Kagami et al. 2010).”
BackgroundTh17 cells confer long-term adaptive immunity to oral mucosal Candida albicans infections
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 191 · see citing works
“Indeed, models of dermal candidiasis implicate innate gd T cells rather than adaptive IL-17-expressing cells.(42,46) However, surprisingly little is known about oral mucosal immunity in mice or how accurately such responses translate to humans.”
BackgroundLeibundGut‐Landmann, S., Wüthrich, M., & Hohl, T. M. (2012) · Current Opinion in Immunology · doi:10.1016/j.coi.2012.04.007 · Cited by 186 · see citing works
“albicans [23,56,57], and pulmonary infection with H.”
Conti, H. R., Bruno, V. M., Childs, E. E., Daugherty, S., Hunter, J. P., Mengesha, B. G., Saevig, D. L., Hendricks, M. R., Coleman, B. M., Brane, L., et al. (2016) · Cell Host & Microbe · doi:10.1016/j.chom.2016.10.001 · Cited by 177 · see citing works
“Mice lacking IL-17RA or IL-17RC are susceptible to OPC and dermal candidiasis (Conti et al., 2009; Conti et al., 2015; Ho et al., 2010; Kagami et al., 2010).”
BackgroundKatt, J., Schwinge, D., Schoknecht, T., Quaas, A., Sobottka, I., Burandt, E., Becker, C., Neurath, M. F., Lohse, A. W., Herkel, J., et al. (2013) · Hepatology · doi:10.1002/hep.26447 · Cited by 175 · see citing works
Okada, S., Asano, T., Moriya, K., Boisson‐Dupuis, S., Kobayashi, M., Casanova, J., & Puel, A. (2020) · Journal of Clinical Immunology · doi:10.1007/s10875-020-00847-x · Cited by 172 · see citing works
Immunity to infection in IL ‐17‐deficient mice and humans
Cypowyj, S., Pïcard, C., Maródi, L., Casanova, J., & Puel, A. (2012) · European Journal of Immunology · doi:10.1002/eji.201242605 · Cited by 169 · see citing works
Chronic mucocutaneous candidiasis disease associated with inborn errors of IL‐17 immunity
Okada, S., Puel, A., Casanova, J., & Kobayashi, M. (2016) · Clinical & Translational Immunology · doi:10.1038/cti.2016.71 · Cited by 175 · see citing works
Candida albicans and Candida glabrata : global priority pathogens
Katsipoulaki, M., Stappers, M. H. T., Malavia, D., Brunke, S., Hube, B., & Gow, N. A. R. (2024) · Microbiology and Molecular Biology Reviews · doi:10.1128/mmbr.00021-23 · Cited by 174 · see citing works
“In mice, deficiency in the IL-17/IL-17R axis and its signaling components is associated with increased susceptibil ity to mucosal (359, 360), skin (361), and systemic candidiasis (357).”
BackgroundIvanov, S., Renneson, J., Fontaine, J., Barthélémy, A., Paget, C., Fernandez, É. M., Blanc, F., Trez, C. D., Maele, L. V., Dumoutier, L., et al. (2013) · Journal of Virology · doi:10.1128/jvi.02943-12 · Cited by 159 · see citing works
Interaction of Candida Species with the Skin
Kühbacher, A., Burger‐Kentischer, A., & Rupp, S. (2017) · Microorganisms · doi:10.3390/microorganisms5020032 · Cited by 161 · see citing works
“Moreover, together with TNF-α, IL-22 induces S100A7, human β-defensin 2, and the antimicrobial chemokines CXCL9, 10, and 11 in keratinocytes in vitro [77,78], yet the role of IL-22 in the defense of CMC is controversial [79].”
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 151 · see citing works
“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 150 · see citing works
“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
Li, J. L. Y., Casanova, J., & Puel, A. (2017) · Mucosal Immunology · doi:10.1038/mi.2017.97 · Cited by 147 · see citing works
“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
Huppler, A. R., Bishu, S., & Gaffen, S. L. (2012) · Arthritis Research & Therapy · doi:10.1186/ar3893 · Cited by 142 · see citing works
“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 146 · see citing works
“…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 137 · see citing works
“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 133 · see citing works
“In addition, IL22 exhibit mild role in protecting against cutaneous candidiasis in mice (98).”
BackgroundGessner, M. A., Werner, J. L., Lilly, L. M., Nelson, M. P., Metz, A. E., Dunaway, C. W., Chan, Y. R., Ouyang, W., Brown, G. D., Weaver, C. T., et al. (2011) · Infection and Immunity · doi:10.1128/iai.05939-11 · Cited by 130 · see citing works
“In models of oral infection (8) and skin infection (18) with C.”
BackgroundDrummond, R. A., & Lionakis, M. S. (2016) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2016.00039 · Cited by 133 · see citing works
Conti, H. R., Huppler, A. R., Whibley, N., & Gaffen, S. L. (2014) · Current Protocols in Immunology · doi:10.1002/0471142735.im1906s105 · Cited by 127 · see citing works
“Dermal candidiasis: The standard dermal model recommends monitoring mice three times a week for healing (Kagami et al., 2010).”
BackgroundInfluentialSafety of secukinumab in the treatment of psoriasis
Blauvelt, A. (2016) · Expert Opinion on Drug Safety · doi:10.1080/14740338.2016.1221923 · Cited by 126 · see citing works
“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
Gaffen, S. L., Hernández‐Santos, N., & Peterson, A. (2011) · Immunologic Research · doi:10.1007/s12026-011-8226-x · Cited by 120 · see citing works
“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 · see citing works
Adaptive Immunity to FungiPreprint
Verma, A. H., Wüthrich, M. D., Deepe, G. S., & Klein, B. S. (2014) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a019612 · Cited by 119 · see citing works
“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 117 · see citing works
“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 116 · see citing works
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 122 · see citing works
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 116 · see citing works
“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 · see citing works
Astry, B., Venkatesha, S. H., & Moudgil, K. D. (2015) · Cytokine · doi:10.1016/j.cyto.2014.11.020 · Cited by 107 · see citing works
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 104 · see citing works
“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 · see citing works
“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 104 · see citing works
The Gut-Liver Axis in Cholestatic Liver Diseases
Blesl, A., & Stadlbauer, V. (2021) · Nutrients · doi:10.3390/nu13031018 · Cited by 99 · see citing works
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 · see citing works
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 93 · see citing works
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 90 · see citing works
“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 88 · see citing works
“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 86 · see citing works
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 86 · see citing works
“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 73 · see citing works
“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 · see citing works
“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 · see citing works
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 71 · see citing works
“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 · see citing works
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 68 · see citing works
“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 · see citing works
“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 65 · see citing works
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 63 · see citing works
“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 · see citing works
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 62 · see citing works
“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 · see citing works
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 · see citing works
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 57 · see citing works
“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 57 · see citing works
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 · see citing works
“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 · see citing works
The role of pattern recognition receptors in the innate recognition ofCandida albicans
Zheng, N.-X., Wang, Y., Hu, D., Yan, L., & Jiang, Y. (2015) · Virulence · doi:10.1080/21505594.2015.1014270 · Cited by 55 · see citing works
“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 · see citing works
“development [30].”
Smeekens, S. P., Gresnigt, M. S., Becker, K. L., Cheng, S., Netea, S. A., Jacobs, L., Jansen, T., van de Veerdonk, F. L., Williams, D. L., Joosten, L. A. B., et al. (2014) · Cytokine · doi:10.1016/j.cyto.2014.10.013 · Cited by 55 · see citing works
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 · see citing works
Self-citationLing, Y., & Puel, A. (2014) · Actas Dermo-Sifiliográficas · doi:10.1016/s0001-7310(14)70016-x · Cited by 53 · see citing works
Nakada, T., Russell, J. A., Boyd, J. H., & Walley, K. R. (2011) · Critical Care · doi:10.1186/cc10515 · Cited by 54 · see citing works
“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 · see citing works
Srivastava, A., Yadav, T. C., Khera, H. K., Mishra, P., Raghuwanshi, N., Pruthi, V., & Prasad, R. (2021) · Journal of Autoimmunity · doi:10.1016/j.jaut.2021.102614 · Cited by 53 · see citing works
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 53 · see citing works
Ricardo, J. W., & Lipner, S. R. (2020) · Dermatologic Therapy · doi:10.1111/dth.13687 · Cited by 49 · see citing works
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 47 · see citing works
“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 48 · see citing works
- 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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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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