ArticleImmunity2015
A critical role for transcription factor Smad4 in T cell function that is independent of transforming growth factor β receptor signaling.
Article in Immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 59 citations in OpenAlex.
- TIF1γ regulates stability of regulatory T cells during inflammation.Nature immunology · 2026Article
- SKI is critical to counter TGF-β signaling to promote T cell function and autoimmunity.Science advances · 2026Article
- Adipose-derived mesenchymal stem cell-exosomes attenuate lipopolysaccharide-induced acute lung injury in mice by regulating the TGFBR2/Smad4 axis to suppress NLRP3-mediated macrophage M1 polarization and pyroptosis.Frontiers in immunology · 2026Article
- Smad4 and Eomes converge on a shared transcriptional program associated with inflammatory CD8 T-cell differentiation.Frontiers in immunology · 2026Article
- Expanding the immune-related targetome of miR-155-5p by integrating time-resolved RNA patterns into miRNA target prediction.RNA biology · 2025Review
- Brief Disruption of Circadian Rhythms Alters Intestinal Barrier Integrity and Modulates DSS-Induced Colitis Severity in Mice.Inflammation · 2025Article
- Kurarinone regulates Th17/Treg balance and ameliorates autoimmune uveitis via Rac1 inhibition.Journal of advanced research · 2025Article
- The multifaceted role of SMAD4 in immune cell function.Biochemistry and biophysics reports · 2025Review
- SMAD4 Regulates the Expression of LCK Affecting Chimeric Antigen Receptor-T Cells Proliferation Through PI3K/Akt Signaling Pathway.Journal of cellular physiology · 2025Article
- Profiling Genome-Wide Methylation Patterns in Cattle Infected withInternational journal of molecular sciences · 2024Article
- Article
- Distinctive multicellular immunosuppressive hubs confer different intervention strategies for left- and right-sided colon cancers.Cell reports. Medicine · 2024Article
- Hepatocyte-specific Smad4 deficiency inhibits hepatocarcinogenesis by promoting CXCL10/CXCR3-dependent CD8Theranostics · 2024Article
- CircLDLRAD3 inhibits Oral squamous cell carcinoma progression by regulating miR-558/Smad4/TGF-β.Journal of cellular and molecular medicine · 2023Article
- Cellular and molecular waypoints along the path of T cell exhaustion.Science immunology · 2023Review
- Intricacies of TGF-β signaling in Treg and Th17 cell biology.Cellular & molecular immunology · 2023Review
- The diverse effects of transforming growth factor-β and SMAD signaling pathways during the CTL response.Frontiers in immunology · 2023Review
- The effect of SMAD4 on the prognosis and immune response in hypopharyngeal carcinoma.Frontiers in medicine · 2023Article
- Exploring the relevance of NUP93 variants in steroid-resistant nephrotic syndrome using next generation sequencing and a fly kidney model.Pediatric nephrology (Berlin, Germany) · 2022Article
- Early fish domestication affects methylation of key genes involved in the rapid onset of the farmed phenotype.Epigenetics · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Transforming growth factor-beta (TGF-β) suppresses T cell function to maintain self-tolerance and to promote tumor immune evasion. Yet how Smad4, a transcription factor component of TGF-β signaling, regulates T cell function remains unclear. Here we have demonstrated an essential role for Smad4 in promoting T cell function during autoimmunity and anti-tumor immunity. Smad4 deletion rescued the lethal autoimmunity resulting from transforming growth factor-beta receptor (TGF-βR) deletion and compromised T-cell-mediated tumor rejection. Although Smad4 was dispensable for T cell generation, homeostasis, and effector function, it was essential for T cell proliferation after activation in vitro and in vivo. The transcription factor Myc was identified to mediate Smad4-controlled T cell proliferation. This study thus reveals a requirement of Smad4 for T-cell-mediated autoimmunity and tumor rejection, which is beyond the current paradigm. It highlights a TGF-βR-independent role for Smad4 in promoting T cell function, autoimmunity, and anti-tumor immunity.
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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.