An ACT1 mutation selectively abolishes interleukin-17 responses in humans with chronic mucocutaneous candidiasis
Open accessAbstract
Patients with inborn errors of interleukin-17F (IL-17F) or IL-17RA display chronic mucocutaneous candidiasis (CMC). We report a biallelic missense mutation (T536I) in the adaptor molecule ACT1 in two siblings with CMC. The mutation, located in the SEFIR domain, abolished the homotypic interaction of ACT1 with IL-17 receptors, with no effect on homodimerization. The patients' fibroblasts failed to respond to IL-17A and IL-17F, and their T cells to IL-17E. By contrast, healthy individuals homozygous for the common variant D10N, located in the ACT1 tumor necrosis factor receptor-associated factor-interacting domain and previously associated with psoriasis, had impaired, but not abolished, responses to IL-17 cytokines. SEFIR-independent interactions of ACT1 with other proteins, such as CD40, heat shock protein 70 (HSP70) and HSP90, were not affected by the T536I mutation. Overall, human IL-17A and IL-17F depend on ACT1 to mediate protective mucocutaneous immunity. Moreover, other ACT1-dependent IL-17 cytokines seem to be largely redundant in host defense.
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IL-17 receptor signaling plays an indispensable role in mucocutaneous host defense against fungi in mice and humans.
“IL-17 receptor (IL-17R) signaling is well-recognized to play an indispensable role in mucocutaneous host defense against fungi (including Candida species) in mice and humans (Boisson et al., 2013; Conti et al., 2016; Lionakis and Levitz, 2018; Puel et al., 2011).”
From Murine model of colonization with fungal pathogen Candida auris to explore skin tropism, host risk factors and therapeutic strategies (2021) · cites this paper as Boisson et al., 2013
The Introduction (page unavailable) states that IL-17A and IL-17F are essential for protective mucocutaneous immunity to C. albicans in humans, and reports chronic mucocutaneous candidiasis in patients with impaired IL-17 signaling. The Discussion mentions IL-17 signaling in mice, but its mouse infection examples concern bacteria and worms, not mucocutaneous fungal defense. The claim’s extension to mice is therefore not supported by this paper’s text. (LLM, conf=0.87)
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- Authors
- Boisson, B., Wang, C., Pedergnana, V., Wu, L., Cypowyj, S., Rybojad, M., Belkadi, A., Picard, C., Abel, L., Fieschi, C., Puel, A., Li, X., & Casanova, J.-L.
- Affiliations
- Rockefeller University (US)
- Cleveland Clinic (US)
- Inserm (FR)
- Hôpital Saint-Louis (FR)
- Hôpital Necker-Enfants Malades (FR)
- Corresponding author
- Boisson, Bertrand
- Casanova, Jean-Laurent
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2013-10
- Volume
- 39
- Issue
- 4
- Pages
- 676-686
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC3873857
- OpenAlex
- W1998541797
- Cited by
- 293
- References
- 11
- Citations by year
- 2026: 9 · 2025: 16 · 2024: 8 · 2023: 23 · 2022: 17 · 2021: 34 · 2020: 35 · 2019: 19 · 2018: 21 · 2017: 31 · 2016: 25 · 2015: 29 · 2014: 22 · 2013: 3
- FWCI
- 14.58
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Funders
- St. Giles Foundation
- AXA Research Fund
- National Institutes of Health (UL1TR000043, 1r01ns071996-01a1, UL1TR000004)
- National Institute of General Medical Sciences (T32GM007250)
- National Institute of Allergy and Infectious Diseases (T32AI089474)
- National Institute of Neurological Disorders and Stroke (R01-NS071996)
- National Center for Research Resources
- National Center for Advancing Translational Sciences (8UL1TR00004)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- Act1, chronic mucocutaneous candidiasis, IL-17, IL-17F, IL-17A, IL-25, missense mutations, IL-17 receptor signaling, T cell response, fibroblast response, CD40, HSP70, HSP90, cytokine redundancy, primary immunodeficiency
- MeSH terms
- Adult, Amino Acid Sequence, Candidiasis, Chronic Mucocutaneous, Female, Fibroblasts, Heat-Shock Proteins, Homozygote, Humans, Immunity, Innate, Male, Molecular Sequence Data, Pedigree, T-Lymphocytes, Protein Structure, Tertiary, Immunity, Mucosal, CD40 Antigens, Mutation, Missense, Interleukin-17, Siblings, Tumor Necrosis Factor Receptor-Associated Peptides and Proteins, Adaptor Proteins, Signal Transducing, Receptors, Interleukin-17, Protein Multimerization
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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