Differential developmental requirement and peripheral regulation for dermal Vγ4 and Vγ6T17 cells in health and inflammation
Open accessAbstract
Dermal IL-17-producing γδT cells have a critical role in skin inflammation. However, their development and peripheral regulation have not been fully elucidated. Here we demonstrate that dermal γδT cells develop from the embryonic thymus and undergo homeostatic proliferation after birth with diversified TCR repertoire. Vγ6T cells are bona fide resident, but precursors of dermal Vγ4T cells may require extrathymic environment for imprinting skin-homing properties. Thymic Vγ6T cells are more competitive than Vγ4 for dermal γδT cell reconstitution and TCRδ(-/-) mice reconstituted with Vγ6 develop psoriasis-like inflammation after IMQ-application. Although both IL-23 and IL-1β promote Vγ4 and Vγ6 proliferation, Vγ4 are the main source of IL-17 production that requires IL-1 signalling. Mice with deficiency of IL-1RI signalling have significantly decreased skin inflammation. These studies reveal a differential developmental requirement and peripheral regulation for dermal Vγ6 and Vγ4 γδT cells, implying a new mechanism that may be involved in skin inflammation.
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Homozygous CCR10-KO/EGFP-KI mice have dysregulated skin-resident T cells compared to heterozygous mice, characterized mostly by reduction of CD8+ and CD4+ αβT cells but not IL-17A+ αβT or γδT cells.
“Homozygous CCR10-KO/EGFP-KI (CCR10EGFP/EGFP, or CCR10−/− for simplicity) mice have dysregulated skin-resident T cells compared to heterozygous CCR10-KO/EGFP-KI (CCR10+/EGFP or CCR10+/−) mice, characterized mostly by the reduction of CD8+ and CD4+ αβT cells but not IL-17A+ αβT or γδT cells.20,22,23”
From Skin-resident T cells play an important role in controlling skin colonization of Candidozyma (Candida) auris (2026) · cites this paper as [23]
The Results section, ‘Thymic Vγ4 requires extrathymic environment for skin homing’ (page unavailable), reports that CCR10 deficiency did not reduce dermal Vγ4 cells relative to wild-type mice and that total dermal γδT-cell frequency was unchanged. The paper does not report the claimed reductions in CD8+ and CD4+ αβT cells or compare homozygous CCR10-KO/EGFP-KI mice with heterozygous mice. (LLM, conf=0.84)
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- Authors
- Cai, Y., Xue, F., Fleming, C., Yang, J., Ding, C., Ma, Y., Liu, M., Zhang, H.-G., Zheng, J., Xiong, N., & Yan, J.
- Affiliations
- University of Louisville (US)
- Shanghai Jiao Tong University (CN)
- Pennsylvania State University (US)
- Corresponding author
- Yan, Jun
- ORCID
- Venue
- Nature Communications
- Published
- 2014-06-09
- Volume
- 5
- Issue
- 1
- Pages
- 11354-11354
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4068267
- OpenAlex
- W2161972318
- Cited by
- 162
- References
- 44
- Citations by year
- 2026: 11 · 2025: 12 · 2024: 12 · 2023: 19 · 2022: 14 · 2021: 7 · 2020: 21 · 2019: 14 · 2018: 10 · 2017: 16 · 2016: 8 · 2015: 14 · 2014: 3
- FWCI
- 6.25
- Type
- journal article
- Language
- en
- Update notices
- correction (2016-04-11)
- Open access
- bronze
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Psoriasis Foundation
- National Institutes of Health
- National Cancer Institute (R01CA150947)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Keywords
- Vγ4 T cells, IL-17, skin inflammation, thymus development, skin homing, T cell receptor repertoire, IL-23, IL-1 signaling, homeostatic proliferation
- MeSH terms
- Animals, Inflammation, Interleukin-1, Mice, Inbred C57BL, Skin, Signal Transduction, Receptors, Antigen, T-Cell, gamma-delta, Mice, Knockout, Interleukin-17, Cell Proliferation, Mice
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