ArticleNature medicine2015
Glucocorticoid-induced tumor necrosis factor receptor-related protein co-stimulation facilitates tumor regression by inducing IL-9-producing helper T cells.
Article in Nature medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
95 citing papers in PubMed, 1 synthesis or guideline pooled it, 162 citations in OpenAlex.
- In or out of control: Modulating regulatory T cell homeostasis and function with immune checkpoint pathways.Frontiers in immunology · 2022Pooled it
- First-in-Human Phase I/II Study of INCAGN01876, a Glucocorticoid-Induced Tumor Necrosis Factor Receptor Agonist, in Patients with Advanced or Metastatic Solid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Trial
- Review
- Th9 cells at the intersection of IBD and colorectal cancer: a context-dependent factor in carcinogenesis.Inflammation and regeneration · 2026Review
- Agonistic GITR treatment enhances antitumor immune responses and suppresses tumor progression in pancreatic ductal adenocarcinoma.Journal of gastroenterology · 2026Article
- Glucocorticoid-Induced TNFR-Related Ligand as a Biomarker for Diagnosis and Severity of Asthma in Children.Pediatric discovery · 2026Article
- Mast cells act as pro-angiogenic and pro-tumorigenic players in pituitary gonadotroph tumors.Neuro-oncology · 2026Article
- Ligand non-competitive GITR antibody prevents formation of the obligatory signal-triggering GITRL: GITR stoichiometry.Scientific reports · 2025Article
- Article
- Sorafenib-treated Th9 cells exhibit superior anti-tumor effect in lung metastasis.Scientific reports · 2025Article
- GITRL enhances cytotoxicity and persistence of CAR-T cells in cancer therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Systemic 4-1BB stimulation augments extrafollicular memory B cell formation and recall responses during Plasmodium infection.Cell reports · 2025Article
- Regulatory mechanisms of Th9 cell differentiation.Frontiers in immunology · 2025Review
- Th9 cells provide protective TB immunity.Frontiers in immunology · 2025Article
- Natural lung-tropic TJournal for immunotherapy of cancer · 2024Article
- Functional diversity and regulation of IL-9-producing T cells in cancer immunotherapy.Cancer letters · 2024Review
- Sphingosylphosphorylcholine Promotes Th9 Cell Differentiation Through Regulation of Smad3, STAT5, and β-Catenin Pathways.Immune network · 2024Article
- PU.1 eviction at lymphocyte-specific chromatin domains mediates glucocorticoid response in acute lymphoblastic leukemia.Nature communications · 2024Article
- Review
- Emerging Roles of Adaptive Immune Response in Alzheimer's Disease.Aging and disease · 2024Review
35 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T cell stimulation via glucocorticoid-induced tumor necrosis factor receptor (TNFR)-related protein (GITR) elicits antitumor activity in various tumor models; however, the underlying mechanism of action remains unclear. Here we demonstrate a crucial role for interleukin (IL)-9 in antitumor immunity generated by the GITR agonistic antibody DTA-1. IL-4 receptor knockout (Il4ra(-/-)) mice, which have reduced expression of IL-9, were resistant to tumor growth inhibition by DTA-1. Notably, neutralization of IL-9 considerably impaired tumor rejection induced by DTA-1. In particular, DTA-1-induced IL-9 promoted tumor-specific cytotoxic T lymphocyte (CTL) responses by enhancing the function of dendritic cells in vivo. Furthermore, GITR signaling enhanced the differentiation of IL-9-producing CD4(+) T-helper (TH9) cells in a TNFR-associated factor 6 (TRAF6)- and NF-κB-dependent manner and inhibited the generation of induced regulatory T cells in vitro. Our findings demonstrate that GITR co-stimulation mediates antitumor immunity by promoting TH9 cell differentiation and enhancing CTL responses and thus provide a mechanism of action for GITR agonist-mediated cancer immunotherapies.
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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.