ArticleJournal of immunotoxicology2014
Modulation of bone morphogenic protein signaling in T-cells for cancer immunotherapy.
Article in Journal of immunotoxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
12 citing papers in PubMed, 17 citations in OpenAlex.
- SMAD4 TGF-β-independent function preconditions naive CD8+ T cells to prevent severe chronic intestinal inflammation.The Journal of clinical investigation · 2022Article
- Bone Morphogenetic Proteins Shape TFrontiers in immunology · 2022Review
- Bone morphogenetic proteins, activins, and growth and differentiation factors in tumor immunology and immunotherapy resistance.Frontiers in immunology · 2022Review
- Bone Morphogenetic Protein Signaling in Cancer; Some Topics in the Recent 10 Years.Frontiers in cell and developmental biology · 2022Review
- Specific Blockade of Bone Morphogenetic Protein-2/4 Induces Oligodendrogenesis and Remyelination in Demyelinating Disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- BMPR2 expression level is correlated with low immune infiltration and predicts metastasis and poor survival in osteosarcoma.Oncology letters · 2021Article
- Regulation of the Immune System in Health and Disease by Members of the Bone Morphogenetic Protein Family.Frontiers in immunology · 2021Review
- Understanding Gene Expression and Transcriptome Profiling of COVID-19: An Initiative Towards the Mapping of Protective Immunity Genes Against SARS-CoV-2 Infection.Frontiers in immunology · 2021Article
- Inhibition of the BMP Signaling Pathway Ameliorated Established Clinical Symptoms of Experimental Autoimmune Encephalomyelitis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Article
- Myelination in Multiple Sclerosis Lesions Is Associated with Regulation of Bone Morphogenetic Protein 4 and Its Antagonist Noggin.International journal of molecular sciences · 2019Article
- TGF-β-mediated enhancement of TScience signaling · 2018Article
- Bone Morphogenetic Protein Signaling Regulates Development and Activation of CD4(+) T Cells.Vitamins and hormones · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Immunotherapy is becoming an increasingly attractive therapeutic alternative for conventional cancer therapy. In recent years Foxp3(+) regulatory T-cells (T(R)) were identified as the major obstacle to effective cancer immunotherapy. The abundance of these cells in peripheral blood is increased in patients with multiple types of cancer and their prevalence among tumor-infiltrating lymphocytes correlated with poor clinical prognosis. In contrast, removal or inactivation of T(R) cells led to enhanced anti-tumor immune response and better efficacy of cancer vaccines. This study reports that Bone Morphogenic Protein Receptor 1α (BMPR1α, Alk-3) is expressed by activated effector CD4(+) and T(R) cells and modulates functions of both cell types. Bone Morphogenic Proteins (BMPs) belong to the transforming growth factor (TGF)-β family of cytokines that also include TGFβ and activins. BMPs play crucial roles in embryonic development, tissue differentiation and homeostasis, and development of cancer. It was demonstrated that BMPs and activins synergize with TGFβ to regulate thymic T-cell development, maintain T(R) cells, and control peripheral tolerance. Inactivation of BMPR1α in T-cells results in impaired thymic and peripheral generation of T(R) cells. BMPR1α-deficient activated T-cells produced a higher level of interferon (IFN)-γ than BMPR1α-sufficient T-cells. Moreover, transplanted B16 melanoma tumors grew smaller in mice lacking expression of BMPR1α in T-cells and tumors had few infiltrating TR cells and a higher proportion of CD8(+) T-cells than wild-type mice.
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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.