Th17 cells are long lived and retain a stem cell-like molecular signature
Open accessAbstract
Th17 cells have been described as short lived, but this view is at odds with their capacity to trigger protracted damage to normal and transformed tissues. We report that Th17 cells, despite displaying low expression of CD27 and other phenotypic markers of terminal differentiation, efficiently eradicated tumors and caused autoimmunity, were long lived, and maintained a core molecular signature resembling early memory CD8(+) cells with stem cell-like properties. In addition, we found that Th17 cells had high expression of Tcf7, a direct target of the Wnt and β-catenin signaling axis, and accumulated β-catenin, a feature observed in stem cells. In vivo, Th17 cells gave rise to Th1-like effector cell progeny and also self-renewed and persisted as IL-17A-secreting cells. Multipotency was required for Th17 cell-mediated tumor eradication because effector cells deficient in IFN-γ or IL-17A had impaired activity. Thus, Th17 cells are not always short lived and are a less-differentiated subset capable of superior persistence and functionality.
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Despite phenotypic markers of terminal differentiation, Th17 cells have stem cell features and powerful functionalities.
“For example, despite their phenotypic markers of terminal differentiation, Th17 cells have stem cell feature with powerful functionalities [71–73].”
From T cell anergy, exhaustion, senescence, and stemness in the tumor microenvironment (2013) · cites this paper as [72]
Human Th17 cells give rise to distinct Th lineages, as measured by IFNγ and Foxp3+ cell expression, and have heightened self-renewal and survival capabilities.
“Human Th17 cells were shown to give rise to distinct Th lineages, as measured through the expression of IFNγ, and Foxp3+ cells, heightened self-renewal, and survival capabilities [71,72].”
From T cell anergy, exhaustion, senescence, and stemness in the tumor microenvironment (2013) · cites this paper as [72]
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Self-citationSynthetic RORγ agonists regulate multiple pathways to enhance antitumor immunity
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- Authors
- Muranski, P., Borman, Z. A., Kerkar, S. P., Klebanoff, C. A., Ji, Y., Sanchez-Perez, L., Sukumar, M., Reger, R. N., Yu, Z., Kern, S. J., Roychoudhuri, R., Ferreyra, G. A., Shen, W., Durum, S. K., Feigenbaum, L., Palmer, D. C., Antony, P. A., Chan, C.-C., Laurence, A., Danner, R. L., Gattinoni, L., & Restifo, N. P.
- Affiliations
- National Institutes of Health (US)
- National Cancer Institute (US)
- Leidos (United States) (US)
- University of Maryland, Baltimore (US)
- Corresponding author
- Restifo, Nicholas P.
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2011-12
- Volume
- 35
- Issue
- 6
- Pages
- 972-985
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC3246082
- OpenAlex
- W1995391551
- Cited by
- 443
- References
- 82
- Citations by year
- 2026: 5 · 2025: 19 · 2024: 24 · 2023: 37 · 2022: 23 · 2021: 39 · 2020: 25 · 2019: 37 · 2018: 30 · 2017: 32 · 2016: 35 · 2015: 40 · 2014: 33 · 2013: 34 · 2012: 28
- FWCI
- 13.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (Z99 CA999999)
- National Cancer Institute (ZIABC010763, Y99 CA999999, ZIABC011037)
- 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 › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- Th17 cells, cell persistence, stem cell-like properties, TCF1, Wnt/β-catenin signaling, CD27, memory CD8+ T cells, IL-17A, interferon-gamma, tumor eradication, autoimmunity, multipotency, self-renewal
- MeSH terms
- Animals, Cell Differentiation, Cell Survival, Mice, Transgenic, Neoplasms, Stem Cells, T-Lymphocyte Subsets, Tumor Necrosis Factor Receptor Superfamily, Member 7, Th1 Cells, Interleukin-17, Gene Expression Profiling, Mice, Th17 Cells
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