Transforming Growth Factor-β Inhibits Interferon-γ Secretion by Lymph okine-activated Killer Cells Stimulated with Tumor Cells
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The effect of transforming growth factor-beta (TGF-beta) secreted by glioblastoma (T98G) cells on the secretion of interferon-gamma (IFN-gamma) by lymphokine-activated killer (LAK) cells stimulated with tumor cells was investigated in cocultures of LAK and Daudi cells supplemented with T98G culture supernatant, T98G culture supernatant preincubated with anti-TGF-beta 1 and anti-TGF-beta 2 neutralizing antibodies, anti-TGF-beta 1 and anti-TGF-beta 2 antibodies, or natural human TGF-beta 1 or recombinant human TGF-beta 2. LAK cells were incubated with anti-TGF-beta 1 and anti-TGF-beta 2 antibodies, and with T98G cells of which the supernatant contained both active and latent forms of TGF-beta 1 and TGF-beta 2, with or without neutralizing antibodies. Addition of the supernatant from T98G cells to LAK/Daudi culture caused inhibition of IFN-gamma secretion by LAK cells. The inhibition was abolished by pretreatment of the supernatants with anti-TGF-beta antibodies. Addition of TGF-beta 1 and TGF-beta 2 to the LAK/Daudi culture inhibited IFN-gamma secretion by LAK cells in a dose-dependent manner. Addition of anti-TGF-beta antibodies to the LAK culture resulted in increased IFN-gamma secretion. T98G cells failed to stimulate LAK cells to secrete more IFN-gamma. Addition of anti-TGF-beta antibodies to the LAK-T98G culture resulted in increased IFN-gamma secretion by LAK cells. These results suggest that most malignant glioma cells which secrete high levels of TGF-beta can inhibit IFN-gamma secretion by LAK cells even after tumor cell stimulation.
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Through Smad signaling, TGF-β lowers IFN-γ, which is needed for myeloid and CD8+ T cell growth and maturation.
“As in other immune cell types, TGF-β/Smad signaling represses interferon-γ (IFN-γ) expression that supports myeloid cell and CD8+ T cell proliferation and differentiation168.”
From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [168]
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TGFβ biology in cancer progression and immunotherapy
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“At an early stage of cancer, TGFβ mitigates myeloid proliferation and differentiation by repressing the expression of cytokine IFNγ.(171,172) Progressively, myeloid cells in advanced-stage cancer produce TGFβ and MMPs that further inhibit antitumor immune reactions and promote tumor metastasis.”
BackgroundNemunaitis, J., Nemunaitis, M., Senzer, N., Snitz, P., Bedell, C., Kumar, P., Pappen, B., Maples, P. B., Shawler, D., & Fakhrai, H. (2009) · Cancer Gene Therapy · doi:10.1038/cgt.2009.15 · Cited by 147 · see citing works
- Authors
- NAGANUMA, H., SASAKI, A., SATOH, E., NAGASAKA, M., NAKANO, S., ISOE, S., TASAKA, K., & NUKUI, H.
- Affiliations
- University of Yamanashi (JP)
- ORCID
- SASAKI, Atsushi
- Venue
- Neurologia medico-chirurgica
- Publisher
- Japan Neurosurgical Society
- Published
- 1996
- Volume
- 36
- Issue
- 11
- Pages
- 789-795
- ISSN
- 0470-8105 (ISSN-L)
- 1349-8029
- OpenAlex
- W2014071641
- Cited by
- 42
- References
- 29
- Citations by year
- 2026: 1 · 2024: 2 · 2023: 2 · 2021: 4 · 2020: 1 · 2017: 2 · 2015: 2 · 2014: 1 · 2013: 1 · 2012: 1
- FWCI
- 0.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neurologia medico-chirurgica (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Immune Cell Function and Interaction
- Keywords
- TGF-beta, interferon-gamma, lymphokine-activated killer cells, glioblastoma, TGF-β1, TGF-beta2, tumor immunosuppression, T98G cells, Daudi cells, anti-TGF-beta antibody
- MeSH terms
- Brain Neoplasms, Glioblastoma, Humans, Interferon-gamma, Killer Cells, Natural, Lymphokines, Tumor Cells, Cultured, Transforming Growth Factor beta
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