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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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“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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“As a consequence of impaired IL-17-associated immunity, APECED patients also develop CMC.”
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“In diesem Sinne sind auch Mutationen in Schlüsselgenen der Th17- DifferenzierungundFehlfunktionenderIL-17-Rezeptoren mit einer erhöhten Anfäl- ligkeitfürchronischmukokutaneKandido-sen assoziiert, was die zentrale Bedeutung dieser Immunachse unterstreicht [17, 18].”
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“Consistent with this, human genetic defects directly impacting the IL-17 pathway confer comparable susceptibility to these fungal pathologies (Puel et al, 2010, 2011; Boisson et al, 2013; Hernández-Santos and Gaffen, 2012; Li et al, 2019).”
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Self-citationPrédisposition génétique aux maladies infectieuses chez l’homme
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“Another troublesome clinical condition is CMC (chronic mucocutaneous candidiasis) secondary to various underlying medical diseases, including impaired T cell function related to dysfunction in interleukin 17 immunity [3].”
BackgroundLe contrôle génétique des maladies infectieuses : des lois de Mendel au séquençage de l’exome
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BackgroundEdwards, T. N., Zhang, S., Liu, A. W., Cohen, J. A., Zhou, P. Y., Mogavero, S., Hube, B., Berman, J. G., Bougnoux, M., Mathers, A. R., et al. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.01.27.921049 · Cited by 2
“mucocutaneous candidiasis [3].”
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“Patients with IL-17 F mutation are highly susceptible to candida infections and exhibit chronic mucocutaneous candidiasis [26].”
BackgroundDefects in intrinsic and innate immunity
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Cytokine networks in Paneth cell regulation
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“Mechanistically, the role of IL-17, independent from IL-23, in the gut is complex and is known to promote defense against pathogenic fungi and bacteria [59], likely at least partially via IL-17 promotion of PC AMP function to control these microbial populations.”
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InfluentialPatogeneza i leczenie zakażeń Candida spp.
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New Findings in Genodermatoses
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“…revealed a negative causal impact of asthma on γδ T cells, possibly reflecting an immune negative feedback mechanism that modulates excessive inflammation. γδ T cells secrete IFN-γ, IL-4, IL-10, and IL-17, which regulate mucosal defense and airway remodeling (Conti et al. 2014; Puel et al. 2011).”
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Immunodeficiencies at the Interface of Innate and Adaptive Immunity
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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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