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Chronic Mucocutaneous Candidiasis in Humans with Inborn Errors of Interleukin-17 Immunity
Open accessAbstract
Chronic yeast infections in the absence of other infections result from genetic deficiencies in proinflammatory host responses.
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In the citing paper
“IL-17-mediated immunity is central to mucocutaneous host defense against fungi such as C. albicans and Malassezia [10,99,100].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [99]
Experimental — accuracy not yet measuredIn the citing paper
“analysis of Th17 cells in different tissue sites has revealed that Th17 cells may exhibit distinct transcriptional profiles associated with either homeostatic or pathogenic functions”
From TH17 cell heterogeneity and its role in tissue inflammation (2023) · cites this paper as [43]
In the citing paper
“intestinal non-pathogenic/homeostatic Th17 cells specific for segmented filamentous bacteria (SFB) have a transcriptome that differs markedly from the pro-inflammatory Th17 cells elicited by Helicobacter hepaticus (H. hepaticus) in mice defective for induced intestinal Treg cells”
From TH17 cell heterogeneity and its role in tissue inflammation (2023) · cites this paper as [43]
In the citing paper
“In the Il10−/− model of colitis, in which IL-10-deficient mice develop spontaneous microbiota-dependent colitis, Th17 cells were identified as the main immune population mediating the inflammatory immune response [43, 133].”
From TH17 cell heterogeneity and its role in tissue inflammation (2023) · cites this paper as [43]
In the citing paper
“In Helicobacter hepaticus- dependent colitis, pathobiont-specific inflammatory Th17 cells are major mediators of intestinal inflammation [43].”
From TH17 cell heterogeneity and its role in tissue inflammation (2023) · cites this paper as [43]
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InfluentialHuman TYK2 deficiency: Mycobacterial and viral infections without hyper-IgE syndrome
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“Autosomal recessive IL-17RA and autosomal dominant IL-17F deficiencies have been reported in chronic mucocutaneous candidiasis (CMC) patients [131].”
BackgroundDevelopment of interleukin-17-producing γδ T cells is restricted to a functional embryonic wave
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“In humans, it is currently emerging that the cytokines IL-17A and IL-17F are particularly important for control of mucocutaneous infections because their absence or mutations in their signaling pathway lead to chronic mucocutaneous candidiasis (Puel et al., 2011; van de Veerdonk et al., 2011).”
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Backgroundd’Enfert, C., Kaune, A.-K., Alaban, L. R., Chakraborty, S., Cole, N. L., Delavy, M., Kosmala, D., Marsaux, B., Fróis-Martins, R., Morelli, M., et al. (2020) · FEMS Microbiology Reviews · doi:10.1093/femsre/fuaa060 · Cited by 377
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“albicans infects mucosal and epidermal surfaces, causing mucocutaneous candidiasis, or disseminates into the bloodstream, causing life-threatening systemic candidiasis (Plantinga et al., 2012; Puel et al., 2011).”
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“Importantly, defects in the IL-17/IL-23 axis render the host exquisitely susceptible to CMC, highlighting the importance of this pathway in controlling C. albicans infections.”
BackgroundInfluentialAutosomal Dominant STAT3 Deficiency and Hyper-IgE Syndrome
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“This is the case for predisposition to invasive pneumococcal diseases [11], Herpes simplex encephalitis [14] and chronic mucocutaneous candidiasis [15].”
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Inborn errors of human IL-17 immunity underlie chronic mucocutaneous candidiasis
Puel, A., Cypowyj, S., Maródi, L., Abel, L., Pïcard, C., & Casanova, J. (2012) · Current Opinion in Allergy and Clinical Immunology · doi:10.1097/aci.0b013e328358cc0b · Cited by 322
Self-citationEffect of IL-17A blockade with secukinumab in autoimmune diseases
Patel, D. D., Lee, D. M., Kolbinger, F., & Antoni, C. (2012) · Annals of the Rheumatic Diseases · doi:10.1136/annrheumdis-2012-202371 · Cited by 313
“The relevance of IL-17 in host defence has been demonstrated in recent genetic studies of subjects with chronic mucocutaneous candidiasis disease.(12) In this syndrome characterised by recurrent or persistent infections (predominantly with Candida albicans or to a lesser extent Staphylococcus aureus) of the mucosae, n…”
BackgroundBlauvelt, A., Reich, K., Tsai, T., Tyring, S. K., Vanaclocha, F., Kingo, K., Ziv, M., Pinter, A., Vender, R. B., Hugot, S., et al. (2016) · Journal of the American Academy of Dermatology · doi:10.1016/j.jaad.2016.08.008 · Cited by 318
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“Individuals with genetic deficiencies in IL-17A and IL-17F are prone to chronic mucocutaneous candidiasis and possibly Staphylococcus aureus (Puel et al., 2011).”
BackgroundInterleukin-17A and Keratinocytes in Psoriasis
Furue, M., Furue, K., Tsuji, G., & Nakahara, T. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21041275 · Cited by 318
IL-17–Mediated Immunity to the Opportunistic Fungal Pathogen Candida albicans
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“family with autosomal dominant CMC (114).”
Backgroundvan de Kerkhof, P. C. M., Griffiths, C. E. M., Reich, K., Leonardi, C. L., Blauvelt, A., Tsai, T., Gong, Y., Huang, J., Papavassilis, C., & Fox, T. (2016) · Journal of the American Academy of Dermatology · doi:10.1016/j.jaad.2016.03.024 · Cited by 301
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“Among these anti-cytokine auto-Abs, neutralizing auto-Abs against IL-17A and IL-17F phenocopy inborn errors of IL-17A/F and underlie chronicmucocutaneous candidiasis (CMC; Kisand et al., 2010; Puel et al., 2011; Puel et al., 2010).”
BackgroundSelf-citationThe role of Dectin-1 in the host defence against fungal infections
Drummond, R. A., & Brown, G. D. (2011) · Current Opinion in Microbiology · doi:10.1016/j.mib.2011.07.001 · Cited by 303
“CMC, Hyper IgE Syndrome, APECED) [51,52] show an increased susceptibility to mucosal candidiasis.”
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“The IL17RA / fibroblasts used have been described elsewhere (Puel et al., 2011).”
InfluentialSelf-citationTH17 cell heterogeneity and its role in tissue inflammation
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Self-citationLoss of ceramide synthase 3 causes lethal skin barrier disruption
Jennemann, R., Rabionet, M., Gorgas, K., Epstein, S., Dalpke, A. H., Rothermel, U., Bayerle, A., van der Hoeven, F., Imgrund, S., Kirsch, J., et al. (2011) · Human Molecular Genetics · doi:10.1093/hmg/ddr494 · Cited by 283
“chronic mucocutaneous candidiasis disease, for which in most cases the underlying etiology is still unknown (56,57), offers a potential linkage to the CERS3 gene.”
BackgroundA cellular and molecular view of T helper 17 cell plasticity in autoimmunity
Stadhouders, R., Lubberts, E., & Hendriks, R. W. (2017) · Journal of Autoimmunity · doi:10.1016/j.jaut.2017.12.007 · Cited by 298
Recent advances in the IL-17 cytokine family
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Th17 Cells in Immunity and Autoimmunity
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“[142] A.”
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“, 2006), or Th17 cell defects (Ferwerda et al., 2009; Glocker et al., 2009; Puel et al., 2011) are not associated with abnormal VZV or EBV responses, arguing against a role for those defects that are normally observed in AD-HIES as a cause for the diminished capacity to control chronic viruses.”
BackgroundHuman inborn errors of immunity: An expanding universe
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“Overall, core molecular deficiencies of these three groups of patients with HIES involve an impaired ZNF341-and STAT3-dependent IL-6 signal transducer (IL-6ST)–mediated response to IL-6 (allergy and staphylococcal disease) and IL-11 (skeletal anomalies), whereas at least some specific features, such as CMC, are caused…”
BackgroundInfluentialSelf-citationInvasive fungal infection and impaired neutrophil killing in human CARD9 deficiency
Drewniak, A., Gazendam, R. P., Tool, A. T. J., van Houdt, M., Jansen, M. H., van Hamme, J. L., van Leeuwen, E. M. M., Roos, D., Scalais, E., de Beaufort, C. E., et al. (2013) · Blood · doi:10.1182/blood-2012-08-450551 · Cited by 283
“The role of IL-17 in the defense against persistent Candida infection has been directly implicated by the identification of IL-17R and IL-17F mutations in pedigrees suffering from chronic mucocutaneous candidiasis (CMC).(4,5) On the other hand, the innate complement and phagocyte pathways of host immunity against Cand…”
BackgroundCandida albicans interactions with epithelial cells and mucosal immunity
Naglik, J. R., Moyes, D. L., Wächtler, B., & Hube, B. (2011) · Microbes and Infection · doi:10.1016/j.micinf.2011.06.009 · Cited by 277
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Interleukin-17 in chronic inflammatory neurological diseases
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“In humans, mutations in IL-17 signaling genes (ACT1, IL17RA, IL17RC) are associated with chronic mucocutaneous candidiasis (5, 7, 8).”
BackgroundGuidelines for genetic studies in single patients: lessons from primary immunodeficiencies
Casanova, J., Conley, M. E., Seligman, S. J., Abel, L., & Notarangelo, L. D. (2014) · The Journal of Experimental Medicine · doi:10.1084/jem.20140520 · Cited by 255
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Interplay between Candida albicans and the mammalian innate host defense
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“Another line of evidence on the role of Th17 for antifungal defense as well as for the occurrence of chronic mucocutaneous candidiasis in patients with IL-17F or IL-17 receptor deficiencies comes from the dectin-1/CARD9/ Th17 pathway (89).”
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
Regulation of host-microbe interactions at oral mucosal barriers by type 17 immunity
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Brown, A. F., Leech, J. M., Rogers, T. R., & McLoughlin, R. M. (2014) · Frontiers in Immunology · doi:10.3389/fimmu.2013.00507 · Cited by 265
“Inborn errors of Th17 cells seem to underlie CMC (209, 210).”
BackgroundKirkham, B. W., Kavanaugh, A., & Reich, K. (2013) · Immunology · doi:10.1111/imm.12142 · Cited by 247
Old and New Biological Therapies for Psoriasis
Rønholt, K., & Iversen, L. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18112297 · Cited by 241
“Manageable mucocutaneous candida infection is associated with all the IL-17 inhibitors, which is probably due to the key role of IL-17 in the host defense against fungi [127,128].”
BackgroundMiller, L. S., Fowler, V. G., Shukla, S. K., Rose, W. E., & Proctor, R. A. (2019) · FEMS Microbiology Reviews · doi:10.1093/femsre/fuz030 · Cited by 242
“aureus skin infections rather than host defense against bacteremia (Cho et al. 2010; Puel et al. 2011; Montgomery et al. 2014; Chan et al. 2015; Marchitto et al. 2019).”
BackgroundHoefs, S., Mogavero, S., & Hube, B. (2016) · The Journal of Microbiology · doi:10.1007/s12275-016-5514-0 · Cited by 251
“observed in patients exhibiting an autosomal recessive deficiency in the IL-17 cytokine receptor IL-17RA, and autosomal dominant deficiency of IL-17F (Puel et al., 2011).”
BackgroundInfluentialChemin, K., Gerstner, C., & Malmström, V. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.00353 · Cited by 243
“Th17 cells are particularly important in protective immunity against fungal and extracellular bacterial infections (Staphylococcus aureus) (58).”
BackgroundCho, J. S., Guo, Y., Ramos, R. I., Hebroni, F., Plaisier, S. B., Xuan, C., Granick, J. L., Matsushima, H., Takashima, A., Iwakura, Y., et al. (2012) · PLoS Pathogens · doi:10.1371/journal.ppat.1003047 · Cited by 237
“aureus in various mouse models of infection (cutaneous infection, systemic infections, pneumonia and brain abscesses [52– 56]) as well as in humans with hyper-IgE syndrome or with a deficiency in IL-17F or IL-17RA [50,57–60].”
Background
Metadata
- Authors
- Puel, A., Cypowyj, S., Bustamante, J., Wright, J. F., Liu, L., Lim, H. K., Migaud, M., Israel, L., Chrabieh, M., Audry, M., Gumbleton, M., Toulon, A., Bodemer, C., El-Baghdadi, J., Whitters, M., Paradis, T., Brooks, J., Collins, M., Wolfman, N. M., Al-Muhsen, S., Galicchio, M., Abel, L., Picard, C., & Casanova, J.-L.
- Affiliations
- Inserm (FR)
- Rockefeller University (US)
- Pfizer (United States) (US)
- Laboratory of Human Genetics of Infectious Diseases, Necker Branch, Institut National de la Santé et de la Recherche Médicale, U980, and University Paris Descartes, Necker Medical School, 75015 Paris, France.
- SUNY Upstate Medical University (US)
- Hôpital Necker-Enfants Malades (FR)
- Unit of Genetics, Military Hospital of Instruction Mohamed V, Rabat 10000, Morocco.
- Prince Naif Center for Immunology Research, Department of Pediatrics, College of Medicine, King Saud University, Riyadh 11461, Saudi Arabia.
- Victor J. Vilela Children’s Hospital, Rosario, Santa Fe 2000, Argentina.
- Corresponding author
- Puel, Anne
- Cypowyj, Sophie
- Abel, Laurent
- Casanova, Jean-Laurent
- ORCID
- Venue
- Science
- Published
- 2011-04
- Volume
- 332
- Issue
- 6025
- Pages
- 65-68
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3070042
- OpenAlex
- W2034453891
- Cited by
- 1,056
- References
- 30
- Citations by year
- 2026: 26 · 2025: 35 · 2024: 29 · 2023: 54 · 2022: 52 · 2021: 64 · 2020: 76 · 2019: 57 · 2018: 67 · 2017: 84 · 2016: 81 · 2015: 76 · 2014: 94 · 2013: 95 · 2012: 103
- FWCI
- 49.58
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Center for Research Resources (UL1RR024143)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- chronic mucocutaneous candidiasis, IL-17A, Candida albicans, primary immunodeficiency, autosomal recessive inheritance, autosomal dominant inheritance
- MeSH terms
- Candida albicans, Candidiasis, Chronic Mucocutaneous, Child, Child, Preschool, Female, Genes, Dominant, Genes, Recessive, Humans, Male, Molecular Sequence Data, Mutation, Pedigree, Signal Transduction, Interleukin-17, Receptors, Interleukin-17, Th17 Cells
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