Deficiency of Th17 cells in hyper IgE syndrome due to mutations in STAT3
Open accessAbstract
Hyper–immunoglobulin E syndrome (HIES) is a primary immune deficiency characterized by abnormal and devastating susceptibility to a narrow spectrum of infections, most commonly Staphylococcus aureus and Candida albicans. Recent investigations have identified mutations in STAT3 in the majority of HIES patients studied. Despite the identification of the genetic cause of HIES, the mechanisms underlying the pathological features of this disease remain to be elucidated. Here, we demonstrate a failure of CD4+ T cells harboring heterozygous STAT3 mutations to generate interleukin 17–secreting (i.e., T helper [Th]17) cells in vivo and in vitro due to a failure to express sufficient levels of the Th17-specific transcriptional regulator retinoid-related orphan receptor γt. Because Th17 cells are enriched for cells with specificities against fungal antigens, our results may explain the pattern of infection susceptibility characteristic of patients with HIES. Furthermore, they underscore the importance of Th17 responses in normal host defense against the common pathogens S. aureus and C. albicans.
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Th17 cells play an important role in tissue homeostasis, especially in the intestinal mucosa.
“Th17 cells have been found to play an important role in tissue homeostasis, especially in the intestinal mucosa.”
From TH17 cell heterogeneity and its role in tissue inflammation (2023) · cites this paper as [44]
Patients with genetic mutations limiting the levels of IL-17A, such as Job's syndrome, suffer from recurring mucocutaneous infections and ulcers.
“Furthermore, patients with genetic mutations limiting the levels of IL-17A, such as Job's syndrome, suffer from recurring mucocutaneous infections and ulcers.78,79”
From The Innate Immune System in Acute and Chronic Wounds (2016) · cites this paper as [78]
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- Authors
- Ma, C. S., Chew, G. Y. J., Simpson, N., Priyadarshi, A., Wong, M., Grimbacher, B., Fulcher, D. A., Tangye, S. G., & Cook, M. C.
- Affiliations
- Garvan Institute of Medical Research (AU)
- Australian National University (AU)
- 4Department of Paediatrics and Child Health, and
- Children's Hospital at Westmead (AU)
- The Royal Free Hospital (GB)
- Westmead Hospital (AU)
- ORCID
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2008-06-30
- Volume
- 205
- Issue
- 7
- Pages
- 1551-1557
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2442632
- OpenAlex
- W2115779634
- Cited by
- 652
- References
- 37
- Citations by year
- 2026: 7 · 2025: 19 · 2024: 12 · 2023: 19 · 2022: 11 · 2021: 25 · 2020: 34 · 2019: 31 · 2018: 32 · 2017: 31 · 2016: 33 · 2015: 52 · 2014: 49 · 2013: 53 · 2012: 54
- FWCI
- 26.42
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Research Online (University of Wollongong) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Figshare (submittedVersion)
- ANU Open Research (Australian National University) (submittedVersion)
- Funders
- Medical Research Council
- National Health and Medical Research Council
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- hyperimmunoglobulin E syndrome, STAT3 mutations, Th17 cells, IL-17, RORC, CD4+ T cells, primary immunodeficiency, Staphylococcus aureus, Candida albicans, fungal infection susceptibility, host defense
- MeSH terms
- Antigens, Fungal, Candida albicans, Candidiasis, Child, Female, T-Lymphocytes, Helper-Inducer, Humans, Job Syndrome, Male, Staphylococcal Infections, Staphylococcus aureus, Receptors, Cytoplasmic and Nuclear, Interleukin-17, STAT3 Transcription Factor
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