ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Truncated form of TGF-βRII, but not its absence, induces memory CD8+ T cell expansion and lymphoproliferative disorder in mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 45 citations in OpenAlex.
- TGF-β in hematologic malignancies: molecular functions and clinical applications.Frontiers in immunology · 2026Review
- Installation of dominant-negative mutations inMolecular therapy. Oncology · 2025Article
- Installation of Dominant-Negative Mutations inbioRxiv : the preprint server for biology · 2025Article
- Armored bicistronic CAR T cells with dominant-negative TGF-β receptor II to overcome resistance in glioblastoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- TGF-β broadly modifies rather than specifically suppresses reactivated memory CD8 T cells in a dose-dependent manner.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- TGFβ control of immune responses in cancer: a holistic immuno-oncology perspective.Nature reviews. Immunology · 2023Review
- Improved memory CD8 T cell response to delayed vaccine boost is associated with a distinct molecular signature.Frontiers in immunology · 2023Article
- Coming in from the cold: overcoming the hostile immune microenvironment of medulloblastoma.Genes & development · 2022Review
- PSMA-targeting TGFβ-insensitive armored CAR T cells in metastatic castration-resistant prostate cancer: a phase 1 trial.Nature medicine · 2022Article
- TGFβ: Signaling Blockade for Cancer Immunotherapy.Annual review of cancer biology · 2022Article
- Review
- TGFβ suppresses CD8Nature communications · 2020Article
- Chimeric antigen receptors designed to overcome transforming growth factor-β-mediated repression in the adoptive T-cell therapy of solid tumors.Clinical & translational immunology · 2019Review
- Review
- Targeting the TGFβ pathway with galunisertib, a TGFβRI small molecule inhibitor, promotes anti-tumor immunity leading to durable, complete responses, as monotherapy and in combination with checkpoint blockade.Journal for immunotherapy of cancer · 2018Article
- Antigen-specific regulatory T-cell responses to intestinal microbiota.Mucosal immunology · 2017Review
- Regulation of the Immune Response by TGF-β: From Conception to Autoimmunity and Infection.Cold Spring Harbor perspectives in biology · 2017Review
- Ribosome-based quality control of mRNA and nascent peptides.Wiley interdisciplinary reviews. RNA · 2017Review
- Immunoregulation by members of the TGFβ superfamily.Nature reviews. Immunology · 2016Review
- TGF-β receptor maintains CD4 T helper cell identity during chronic viral infections.The Journal of clinical investigation · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammatory and anti-inflammatory cytokines play an important role in the generation of effector and memory CD8(+) T cells. We used two different models, transgenic expression of truncated (dominant negative) form of TGF-βRII (dnTGFβRII) and Cre-mediated deletion of the floxed TGF-βRII to examine the role of TGF-β signaling in the formation, function, and homeostatic proliferation of memory CD8(+) T cells. Blocking TGF-β signaling in effector CD8(+) T cells using both of these models demonstrated a role for TGF-β in regulating the number of short-lived effector cells but did not alter memory CD8(+) T cell formation and their function upon Listeria monocytogenes infection in mice. Interestingly, however, a massive lymphoproliferative disorder and cellular transformation were observed in Ag-experienced and homeostatically generated memory CD8(+) T cells only in cells that express the dnTGFβRII and not in cells with a complete deletion of TGF-βRII. Furthermore, the development of transformed memory CD8(+) T cells expressing dnTGFβRII was IL-7- and IL-15-independent, and MHC class I was not required for their proliferation. We show that transgenic expression of the dnTGFβRII, rather than the absence of TGF-βRII-mediated signaling, is responsible for dysregulated expansion of memory CD8(+) T cells. This study uncovers a previously unrecognized dominant function of the dnTGFβRII in CD8(+) T cell proliferation and cellular transformation, which is caused by a mechanism that is different from the absence of TGF-β signaling. These results should be considered during both basic and translational studies where there is a desire to block TGF-β signaling in CD8(+) T cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.