ArticleThe Journal of clinical investigation2023
Autonomous IL-36R signaling in neutrophils activates potent antitumor effector functions.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 12 citations in OpenAlex.
- Neutrophil-derived exosomes inhibit gastric cancer progression via miR-101-3p-mediated suppression of MCL1.Cancer cell international · 2026Article
- Immune cell-based therapies for solid tumors, current challenges and therapeutic advances.Cell communication and signaling : CCS · 2025Review
- Stromal fibrin shapes immune infiltration landscape of pancreatic ductal adenocarcinoma.Biomaterials · 2025Article
- Epicutaneous Staphylococcus aureus initiates cross-tissue IL-36R signaling for neutrophilic lung inflammation in a model of the atopic march.Cell reports · 2025Article
- Complex I inhibition combined with TLR activation in the breast tumor microenvironment educates cytotoxic neutrophils.Science advances · 2025Article
- Review
- IL-36-related genes predict prognosis of gastric cancer.Frontiers in oncology · 2025Article
- Role of IL-1 Family Cytokines IL-36, IL-37, IL-38 in Osteoarthritis and Rheumatoid Arthritis: A Comprehensive Review.Journal of inflammation research · 2024Review
- Advances in the two-dimensional layer materials for cancer diagnosis and treatment: unique advantages beyond the microsphere.Frontiers in bioengineering and biotechnology · 2023Review
- When Conventional Therapy Fails: Interleukin-36 Inhibition for Severe Hydroxychloroquine-Induced Acute Generalized Exanthematous Pustulosis in Systemic Lupus Erythematosus - A Case Report.Case reports in dermatologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While the rapid advancement of immunotherapies has revolutionized cancer treatment, only a small fraction of patients derive clinical benefit. Eradication of large, established tumors appears to depend on engaging and activating both innate and adaptive immune system components to mount a rigorous and comprehensive immune response. Identifying such agents is a high unmet medical need, because they are sparse in the therapeutic landscape of cancer treatment. Here, we report that IL-36 cytokine can engage both innate and adaptive immunity to remodel an immune-suppressive tumor microenvironment (TME) and mediate potent antitumor immune responses via signaling in host hematopoietic cells. Mechanistically, IL-36 signaling modulates neutrophils in a cell-intrinsic manner to greatly enhance not only their ability to directly kill tumor cells but also promote T and NK cell responses. Thus, while poor prognostic outcomes are typically associated with neutrophil enrichment in the TME, our results highlight the pleiotropic effects of IL-36 and its therapeutic potential to modify tumor-infiltrating neutrophils into potent effector cells and engage both the innate and adaptive immune system to achieve durable antitumor responses in solid tumors.
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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.