Generation of RORγt+ Antigen-Specific T Regulatory 17 Cells from Foxp3+ Precursors in Autoimmunity
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Th17 cells are potent mediators in autoimmune diseases, and RORγt is required for their development. Recent studies have shown that RORγt + Treg cells in the gut regulate intestinal inflammation by inhibiting effector T cell function. In the current study, we report that RORγt + Treg cells were also found in lymph nodes following immunization. Not only distinct from intestinal RORγt + Treg cells in their transcriptomes, peripheral RORγt + Treg cells were derived from Foxp3 + thymic Treg cells in an antigen-specific manner. Development of these RORγt + Treg cells, coined T regulatory 17 (Tr17) cells, depended on IL-6/Stat3 signaling. Tr17 cells showed suppressive activity against antigen-specific effector T cells in vitro. In addition, Tr17 cells efficiently inhibited myelin-specific Th17-cell-mediated CNS auto-inflammation in a passive EAE model. Collectively, our study demonstrates that Tr17 cells are effector Treg cells that potentially restrict autoimmunity.
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Helios, Nrp-1 or ROR-γt are widely accepted for the discrimination of tTreg and pTreg cells under homeostatic conditions.
“Yet, Helios, Nrp-1 or ROR-γt are widely accepted for the discrimination of tTreg and pTreg cells under homeostatic conditions [364-366, 437-440].”
From Guidelines for the use of flow cytometry and cell sorting in immunological studies (third edition) (2021) · cites this paper as [439]
The Discussion (page unavailable) uses Helios and Nrp-1 to distinguish mostly thymic-derived peripheral RORγt+ Treg cells from intestinal RORγt+ cells of peripheral origin. The Results (page unavailable) say RORγt+ Treg cells occur constitutively in the gut, but the paper also finds RORγt+ cells derived from thymic Treg cells after immunization. It therefore supports the marker-based distinction in these settings, not the broader claim that RORγt itself discriminates tTreg from pTreg cells generally under homeostatic conditions. (LLM, conf=0.82)
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- Authors
- Kim, B.-S., Lu, H., Ichiyama, K., Chen, X., Zhang, Y.-B., Mistry, N. A., Tanaka, K., Lee, Y.-H., Nurieva, R., Zhang, L., Yang, X., Chung, Y., Jin, W., Chang, S. H., & Dong, C.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Chinese Academy of Sciences (CN)
- University of Cincinnati (US)
- University of New Mexico (US)
- Seoul National University (KR)
- Tsinghua University (CN)
- Corresponding author
- Chang, Seon Hee
- Dong, Chen
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2017-10
- Volume
- 21
- Issue
- 1
- Pages
- 195-207
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC5716359
- OpenAlex
- W2762184317
- Cited by
- 137
- References
- 45
- Citations by year
- 2026: 12 · 2025: 9 · 2024: 16 · 2023: 15 · 2022: 10 · 2021: 21 · 2020: 20 · 2019: 20 · 2018: 12 · 2017: 2
- FWCI
- 6.67
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Institute of Hydrobiology, CAS Institutional Repository (submittedVersion)
- Funders
- U.S. Department of Defense (W81XWH-16-1-0100)
- Cancer Prevention and Research Institute of Texas (RP130078)
- Ministry of Education (2016R1A6A3A11933284)
- National Research Foundation of Korea
- National Institutes of Health (R01AR050772)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- RORγt, regulatory T cells, Th17 cells, IL-6/STAT3 signaling, experimental autoimmune encephalitis, Treg suppressive function, autoimmunity
- MeSH terms
- Animals, Cell Differentiation, Encephalomyelitis, Autoimmune, Experimental, Gene Expression Regulation, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Transgenic, Peptide Fragments, Signal Transduction, Autoimmunity, Interleukin-6, Genes, Reporter, Adoptive Transfer, Green Fluorescent Proteins, T-Lymphocytes, Regulatory, STAT3 Transcription Factor, Mice, Forkhead Transcription Factors, Receptors, CCR6, Nuclear Receptor Subfamily 1, Group F, Member 3, Th17 Cells, Inducible T-Cell Co-Stimulator Protein, Myelin-Oligodendrocyte Glycoprotein
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