T-helper-1-cell cytokines drive cancer into senescence
Open accessAbstract
Cancer control by adaptive immunity involves a number of defined death and clearance mechanisms. However, efficient inhibition of exponential cancer growth by T cells and interferon-γ (IFN-γ) requires additional undefined mechanisms that arrest cancer cell proliferation. Here we show that the combined action of the T-helper-1-cell cytokines IFN-γ and tumour necrosis factor (TNF) directly induces permanent growth arrest in cancers. To safely separate senescence induced by tumour immunity from oncogene-induced senescence, we used a mouse model in which the Simian virus 40 large T antigen (Tag) expressed under the control of the rat insulin promoter creates tumours by attenuating p53- and Rb-mediated cell cycle control. When combined, IFN-γ and TNF drive Tag-expressing cancers into senescence by inducing permanent growth arrest in G1/G0, activation of p16INK4a (also known as CDKN2A), and downstream Rb hypophosphorylation at serine 795. This cytokine-induced senescence strictly requires STAT1 and TNFR1 (also known as TNFRSF1A) signalling in addition to p16INK4a. In vivo, Tag-specific T-helper 1 cells permanently arrest Tag-expressing cancers by inducing IFN-γ- and TNFR1-dependent senescence. Conversely, Tnfr1(-/-)Tag-expressing cancers resist cytokine-induced senescence and grow aggressively, even in TNFR1-expressing hosts. Finally, as IFN-γ and TNF induce senescence in numerous murine and human cancers, this may be a general mechanism for arresting cancer progression.
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The same group later showed that these arrested cells were arrested due to senescence.
“the same group later showed that these cells were arrested due to senescence 126”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [126]
Adaptive immunity and TH1 T cell cytokines can directly drive cancer cells into senescence.
“Another example involves adaptive immunity and T H 1 T cell cytokines that can directly drive cancer cells into senescence 126”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [126]
IFNγ and TNF induce senescence in a number of different cancers both in vitro and in vivo.
“Braumüller et al. 126 confirmed that IFNγ and TNF induce senescence in a number of different cancers both in vitro and in vivo.”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [126]
In RIP-Tag2 mice, the Th1 cell cytokines IFNγ and TNF cause pancreatic β-cell tumour regression.
“| T H 1 cell cytokines | RIP-Tag2 | | | IFNγ and TNF | Pancreatic β-cell tumour regression | 126 |”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [126]
Cytokines from CD4+ Th1 cells activated by tumour-associated antigen can drive tumours into senescence.
“This study shows that tumours can be induced into senescence by cytokines derived from tumour associated antigen (TAA)-activated CD4+ Th1 cells.”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [126]
TH1 cytokines from CD4+ T cells recruited by senescent hepatocytes carrying mutated NRAS G12V enable macrophage-dependent clearance of pre-malignant cells and reinstate senescence in tumors that bypassed OIS.
“In line with this concept, TH1 cytokines produced by CD4+ T cells-recruited by senescent hepatocytes carrying mutated NRAS G12V-set the ground for the macrophage (M4)-dependent clearance of pre-malignant cells 184 and reinstate senescence in tumors that have bypassed OIS.185”
From Meta-hallmarks of aging and cancer (2023) · cites this paper as [185]
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- Authors
- Braumüller, H., Wieder, T., Brenner, E., Aßmann, S., Hahn, M., Alkhaled, M., Schilbach, K., Essmann, F., Kneilling, M., Griessinger, C., Ranta, F., Ullrich, S., Mocikat, R., Braungart, K., Mehra, T., Fehrenbacher, B., Berdel, J., Niessner, H., Meier, F., van den Broek, M., Häring, H.-U., Handgretinger, R., Quintanilla-Martinez, L., Fend, F., Pesic, M., Bauer, J., Zender, L., Schaller, M., Schulze-Osthoff, K., & Röcken, M.
- Affiliations
- University of Tübingen (DE)
- Helmholtz Munich (DE)
- Corresponding author
- Röcken, Martin
- ORCID
- Wieder, Thomas
- Brenner, Ellen
- Hahn, Matthias
- Alkhaled, Mohammed
- Schilbach, Karin
- Essmann, Frank
- Kneilling, Manfred
- Ullrich, Susanne
- Mocikat, Ralph
- Mehra, Tarun
- Fehrenbacher, Birgit
- Niessner, Heike
- Meier, Friedegund
- Häring, Hans-Ulrich
- Handgretinger, Rupert
- Fend, Falko
- Pesic, Marina
- Bauer, Jürgen
- Zender, Lars
- Schaller, Martin
- Röcken, Martin
- Venue
- Nature
- Published
- 2013-02
- Volume
- 494
- Issue
- 7437
- Pages
- 361-365
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2080641261
- Cited by
- 720
- References
- 7
- Citations by year
- 2026: 24 · 2025: 42 · 2024: 48 · 2023: 75 · 2022: 56 · 2021: 53 · 2020: 54 · 2019: 52 · 2018: 46 · 2017: 57 · 2016: 53 · 2015: 61 · 2014: 59 · 2013: 39 · 2012: 1
- FWCI
- 49.07
- Type
- journal article
- Language
- en
- Open access
- green
- www.zora.uzh.ch
- Licence
- other-oa
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
- RePEc: Research Papers in Economics (submittedVersion)
- Site cant be reached (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- Th1 cells, interferon-gamma, TNF-α, STAT1, TNFR1, p16INK4a, SV40 large T antigen, adaptive immunity, oncogene-induced senescence, growth arrest, cancer control, CDKN2A
- MeSH terms
- Animals, Antigens, Polyomavirus Transforming, Cell Cycle, Disease Models, Animal, Female, Humans, Interferon-gamma, Male, Mice, Transgenic, Neoplasms, Oncogenes, Phosphoserine, Time Factors, Tumor Cells, Cultured, Tumor Necrosis Factor-alpha, Tumor Suppressor Protein p53, Retinoblastoma Protein, Cytokines, Mice, SCID, Mice, Inbred NOD, Cellular Senescence, Th1 Cells, Disease Progression, Cyclin-Dependent Kinase Inhibitor p16, Receptors, Tumor Necrosis Factor, Type I, Cell Proliferation, STAT1 Transcription Factor, Mice
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