Interleukin-17-Producing γδ T Cells Selectively Expand in Response to Pathogen Products and Environmental Signals
Open accessAbstract
Gammadelta T cells are an innate source of interleukin-17 (IL-17), preceding the development of the adaptive T helper 17 (Th17) cell response. Here we show that IL-17-producing T cell receptor gammadelta (TCRgammadelta) T cells share characteristic features with Th17 cells, such as expression of chemokine receptor 6 (CCR6), retinoid orphan receptor (RORgammat), aryl hydrocarbon receptor (AhR), and IL-23 receptor. AhR expression in gammadelta T cells was essential for the production of IL-22 but not for optimal IL-17 production. In contrast to Th17 cells, CCR6(+)IL-17-producing gammadelta T cells, but not other gammadelta T cells, express Toll-like receptors TLR1 and TLR2, as well as dectin-1, but not TLR4 and could directly interact with certain pathogens. This process was amplified by IL-23 and resulted in expansion, increased IL-17 production, and recruitment of neutrophils. Thus, innate receptor expression linked with IL-17 production characterizes TCRgammadelta T cells as an efficient first line of defense that can orchestrate an inflammatory response to pathogen-derived as well as environmental signals long before Th17 cells have sensed bacterial invasion.
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Expression of IL-22 requires AhR.
“it was demonstrated that expression of IL-22 requires the AhR (Martin et al., 2009; Veldhoen et al., 2008).”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as Martin et al., 2009
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Redundant Innate and Adaptive Sources of IL17 Production Drive Colon Tumorigenesis
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The Skin-Resident Immune Network
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Ncf1 polymorphism reveals oxidative regulation of autoimmune chronic inflammation
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Intestinal Barrier Interactions with Specialized CD8 T Cells
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- Authors
- Martin, B., Hirota, K., Cua, D. J., Stockinger, B., & Veldhoen, M.
- Affiliations
- National Institute for Medical Research (GB)
- Corresponding author
- Veldhoen, Marc
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2009-08
- Volume
- 31
- Issue
- 2
- Pages
- 321-330
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2014913358
- Cited by
- 822
- References
- 57
- Citations by year
- 2026: 12 · 2025: 16 · 2024: 27 · 2023: 29 · 2022: 36 · 2021: 32 · 2020: 33 · 2019: 27 · 2018: 41 · 2017: 54 · 2016: 48 · 2015: 53 · 2014: 68 · 2013: 80 · 2012: 86
- FWCI
- 38.18
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Keywords
- γδ T cells, IL-17, Th17 cells, aryl hydrocarbon receptor, CCR6, RORγ, IL-23, IL-22, Toll-like receptors, Dectin-1, innate immunity, neutrophil recruitment, pathogen recognition, environmental cues, inflammation
- MeSH terms
- Interleukin-22, Dectin-1, Animals, Bacterial Infections, T-Lymphocytes, Helper-Inducer, Interleukins, Membrane Proteins, Mice, Inbred C57BL, Nerve Tissue Proteins, Neutrophils, Receptors, Thyroid Hormone, Interleukin-6, T-Lymphocyte Subsets, Receptors, Antigen, T-Cell, gamma-delta, Receptors, Retinoic Acid, Receptors, Aryl Hydrocarbon, Interleukin-17, Lectins, C-Type, Toll-Like Receptor 1, Toll-Like Receptor 2, Mice, Basic Helix-Loop-Helix Proteins, Interleukin-23, Receptors, CCR6, Nuclear Receptor Subfamily 1, Group F, Member 3
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