Human T H 17 Cells Are Long-Lived Effector Memory Cells
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Human T H 17 cells function as long-lived effector memory cells in the context of chronic disease.
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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 [71]
Th17 cells retain a stem cell-like phenotype through coordinated effects of HIF1α/Notch/Bcl-2 and are potent anti-tumor effectors.
“Interestingly, Th17 cells retain a stem cell-like phenotype through the coordinated effects of HIF1α/Notch/Bcl-2 and are also potent anti-tumor effectors [71], suggesting that stemness might correlate with better immune responses.”
From T cell anergy, exhaustion, senescence, and stemness in the tumor microenvironment (2013) · cites this paper as [71]
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 [71]
Human TH17 cells have high self-renewal potential, potent persistence, apoptotic resistance in vivo, and plasticity to convert into other cell types.
“Human TH17 cells were shown to have a high potential for self-renewal, potent persistence, apoptotic resistance in vivo and plasticity to convert into other cell types.”
From T-cell aging in rheumatoid arthritis (2014) · cites this paper as [37]
Human TH17 cells are terminally differentiated memory T cells distinct from central memory and exhausted T cells.
“IL-17 producing TH17 cells, which have recently been characterized as terminally differentiated memory T cells, distinct from both central memory T cells and exhausted T cells.”
From T-cell aging in rheumatoid arthritis (2014) · cites this paper as [37]
The gene signature of TH17 cells includes HIF1a and NOTCH, which together regulate survival gene expression.
“Their typifying gene signature included hypoxia-inducible factor1a and NOTCH which collaboratively regulate expression of survival genes [37].”
From T-cell aging in rheumatoid arthritis (2014) · cites this paper as [37]
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References 35 · Cited by 278
- Authors
- Kryczek, I., Zhao, E., Liu, Y., Wang, Y., Vatan, L., Szeliga, W., Moyer, J., Klimczak, A., Lange, A., & Zou, W.
- Affiliations
- University of Michigan (US)
- Ludwik Hirszfeld Institute of Immunology and Experimental Therapy (PL)
- Corresponding author
- Zou, Weiping
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2011-10-12
- Volume
- 3
- Issue
- 104
- Pages
- 104ra100-104ra100
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC3345568
- OpenAlex
- W2103119361
- Cited by
- 278
- References
- 35
- Citations by year
- 2026: 12 · 2025: 9 · 2024: 13 · 2023: 15 · 2022: 26 · 2021: 12 · 2020: 15 · 2019: 18 · 2018: 15 · 2017: 21 · 2016: 22 · 2015: 30 · 2014: 19 · 2013: 27 · 2012: 21
- FWCI
- 9.93
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (P30-CA 46592, R01CA152470, R01CA156685, P50CA97248, P50CA097248, R01CA099985, P30CA046592)
- 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
- Th17 cells, effector memory T cells, T cell survival, apoptosis resistance, self-renewal, T cell plasticity, Bcl-2 family genes, hypoxia-inducible factor-1α, Notch signaling, graft-versus-host disease, ulcerative colitis, antitumor immunity, adoptive T cell therapy, autoimmune disease, cancer immunotherapy
- MeSH terms
- Animals, Autoimmune Diseases, Cell Differentiation, Gene Expression Regulation, Humans, Immunologic Memory, Phenotype, Cellular Senescence, Apoptosis, Gene Expression Profiling, Cell Line, Tumor, Mice, Hypoxia-Inducible Factor 1, alpha Subunit, Receptors, Notch, Th17 Cells
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