ArticleThe Journal of allergy and clinical immunology2021
Two patients with chronic mucocutaneous candidiasis caused by TRAF3IP2 deficiency.
Article in The Journal of allergy and clinical immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- A Child with Chronic Mucocutaneous Candidiasis Harbors a Novel Gain-of-Function Mutation in STAT1.Journal of clinical immunology · 2025Article
- Human immunity to fungal infections.The Journal of experimental medicine · 2025Review
- Progress in molecular diagnosis and treatment of chronic mucocutaneous candidiasis.Frontiers in immunology · 2024Review
- Isolated Chronic Mucocutaneous Candidiasis due to a Novel Duplication Variant of IL17RC.Journal of clinical immunology · 2023Article
- The Th17/IL-17 Axis and Host Defense Against Fungal Infections.The journal of allergy and clinical immunology. In practice · 2023Review
- Of Mycelium and Men: Inherent Human Susceptibility to Fungal Diseases.Pathogens (Basel, Switzerland) · 2023Review
- A Novel TRAF3IP2 Mutation Causing Chronic Mucocutaneous Candidiasis.Journal of clinical immunology · 2021Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundTRAF3 interacting protein 2 (TRAF3IP2) (Act1) is an adapter protein that interacts with IL-17R via its similar expression to fibroblast growth factor genes and IL-17R domain and coordinates 2 separate proinflammatory pathways following IL-17 cytokine stimulation.
objectiveWe sought to elucidate the immunologic consequences of TRAF3IP2 homozygous mutations to improve treatments for immunodeficiency patients with chronic mucocutaneous candidiasis.
methodsWe describe 2 patients presenting with chronic mucocutaneous candidiasis who harbor biallelic nonsense mutations in TRAF3IP2. The cellular and molecular features of this genetic defect were assessed using in vitro cytokine assays and protein analysis.
resultsWe show that the homozygous mutation causes complete loss of protein expression. We also show that the absence of TRAF3IP2 was associated with a defective response to combined IL-2/IL-25 (IL-17E) stimulation.
conclusionsFailure to initiate normal signaling downstream of IL-17R engagement likely contributes to the patients' recurrent fungal infections. These findings add to our molecular understanding of genetic defects affecting this critical pathway of antifungal immunity.
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