ArticleJCI insight2023
Dual IL-6 and CTLA-4 blockade regresses pancreatic tumors in a T cell- and CXCR3-dependent manner.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 31 citations in OpenAlex.
- Randomized Phase II Study of Nab-Paclitaxel and Gemcitabine With or Without Tocilizumab as First-Line Treatment in Advanced Pancreatic Cancer: Survival and Cachexia.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025Trial
- Article
- Hypoxia-Induced Fibroblast IL-6 Promotes Immunosuppressive Macrophage Phenotypes in Pancreatic Cancer.Cells · 2026Article
- GOT1 Inhibition Induces Extracellular Matrix Remodeling in Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- IL-6 as a central driver of immune evasion in PDAC: from IDO-mediated tolerance to multi-pathway immunosuppression.Frontiers in immunology · 2026Review
- Interleukin-6: The Unexpected Opponent to Pancreatic Cancer.Cellular and molecular gastroenterology and hepatology · 2026Article
- Rethinking PDAC: from immunological silence to therapeutic opportunity.Frontiers in immunology · 2026Review
- Interleukin 6 Drives Durable T Cell-Mediated Immunity to Pancreatic Cancer.Cellular and molecular gastroenterology and hepatology · 2026Article
- Bidirectional regulatory mechanisms and therapeutic prospects of tumor hypercoagulable state and immunosuppressive tumor microenvironment.Oncology reviews · 2026Review
- Bibliometric analysis of global research trends in pancreatic cancer immunotherapy.Human vaccines & immunotherapeutics · 2025Article
- CXCR3 enhanced murine chimeric antigen receptor T cells in the treatment of solid tumors.Translational cancer research · 2025Article
- Role of interleukin-6 in resistance to tumor therapy.Discover oncology · 2025Review
- Review
- Engineered chemokines, resistant to cancer-mediated post-transcriptional modifications, as drugs to improve cancer immunotherapy.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The role of inflammatory factors in the tumor microenvironment of pancreatic cancer.Frontiers in immunology · 2025Review
- The antitumor activity of TGFβ-specific T cells is dependent on IL-6 signaling.Cellular & molecular immunology · 2025Article
- It's about TIME - Gal-9 as a potential immunotherapeutic target in pancreatic ductal adenocarcinoma.Frontiers in immunology · 2025Review
- Development of a nomogram integrating immune checkpoints, fibrosis indicators, and clinicopathological characteristics to predict overall survival in pancreatic cancer: a retrospective analysis.Frontiers in immunology · 2025Article
- PD-L1 restrains PD-1Cell reports · 2024Article
- VPAC2 Receptor Signaling Promotes Growth and Immunosuppression in Pancreatic Cancer.Cancer research · 2024Article
Corrections and comments
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Authors and funding
21 authors at 5 institutions in 1 country.
Funding
Abstract
This study aimed to enhance antitumor immune responses to pancreatic cancer via Ab-based blockade of IL-6 and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4). Mice bearing s.c. or orthotopic pancreatic tumors were treated with blocking Abs to IL‑6 and/or CTLA-4. In both tumor models, dual IL-6 and CTLA-4 blockade significantly inhibited tumor growth. Additional investigations revealed that dual therapy induced an overwhelming infiltration of T cells into the tumor as well as changes in CD4+ T cell subsets. Dual blockade therapy elicited CD4+ T cells to secrete increased IFN-γ in vitro. Likewise, in vitro stimulation of pancreatic tumor cells with IFN-γ profoundly increased tumor cell production of CXCR3-specific chemokines, even in the presence of IL-6. In vivo blockade of CXCR3 prevented orthotopic tumor regression in the presence of the combination treatment, demonstrating a dependence on the CXCR3 axis for antitumor efficacy. Both CD4+ and CD8+ T cells were required for the antitumor activity of this combination therapy, as their in vivo depletion via Abs impaired outcomes. These data represent the first report to our knowledge of IL-6 and CTLA‑4 blockade as a means to regress pancreatic tumors with defined operative mechanisms of efficacy.
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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.