ArticleNature communications2021
PPARɣ drives IL-33-dependent ILC2 pro-tumoral functions.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- The soldiers needed to be awakened: Tumor-infiltrating immune cells.Frontiers in genetics · 2022Pooled it
- Interleukin-33 and its receptor: multifaceted roles and emerging therapeutic potential.Nature reviews. Immunology · 2026Review
- Review
- ILC2s and their immune checkpoints in the antitumor response.Journal for immunotherapy of cancer · 2026Review
- Tumor-infiltrating immature innate lymphoid cells in colorectal cancer are biased toward ILC1/tissue-resident NK cell differentiation.Nature communications · 2026Article
- Mast-cell derived nerve growth factor drives ILC2 pro-tumoral functions in bladder cancer.Nature communications · 2026Article
- Type 2 Inflammatory Diseases: The Crossroads of Immunity and Metabolism.Research (Washington, D.C.) · 2026Review
- Decoding innate lymphoid cell heterogeneity and plasticity in colorectal cancer.Clinical and translational medicine · 2026Article
- Targeting androgen receptor signaling to enhance cancer immunotherapy.Trends in pharmacological sciences · 2025Review
- The immunoproteasome regulates ILC2 responses by modulating mitochondrial capacity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Unlocking IL-33: New Insights into Tumor Immunity.Immune network · 2025Review
- Cellular Cosmetics: How Innate Lymphoid Cells Can Recontour the Tumour Microenvironment.European journal of immunology · 2025Review
- Dendritic Cell-Based Cancer Vaccines: The Impact of Modulating Innate Lymphoid Cells on Anti-Tumor Efficacy.Cells · 2025Review
- Circulating innate lymphoid cells are dysregulated in patients with prostate cancer.Cellular & molecular biology letters · 2025Article
- Lipid metabolism: the potential therapeutic targets in glioblastoma.Cell death discovery · 2025Review
- Regulatory role of PPAR in colorectal cancer.Cell death discovery · 2025Review
- Innate lymphoid cells in the spotlight: from biomarkers to blueprint for innovative immunotherapy.Frontiers in immunology · 2025Review
- Immunometabolic analysis of primary murine group 2 innate lymphoid cells: a robust step-by-step approach.Frontiers in immunology · 2025Article
- Exogenous IL-33 promotes tumor immunity via macroscopic regulation of ILC2s.Scientific reports · 2024Article
- IL-33/NF-κB/ST2L/Rab37 positive-feedback loop promotes M2 macrophage to limit chemotherapeutic efficacy in lung cancer.Cell death & disease · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group 2 innate lymphoid cells (ILC2s) play a critical role in protection against helminths and in diverse inflammatory diseases by responding to soluble factors such as the alarmin IL-33, that is often overexpressed in cancer. Nonetheless, regulatory factors that dictate ILC2 functions remain poorly studied. Here, we show that peroxisome proliferator-activated receptor gamma (PPARγ) is selectively expressed in ILC2s in humans and in mice, acting as a central functional regulator. Pharmacologic inhibition or genetic deletion of PPARγ in ILC2s significantly impair IL-33-induced Type-2 cytokine production and mitochondrial fitness. Further, PPARγ blockade in ILC2s disrupts their pro-tumoral effect induced by IL-33-secreting cancer cells. Lastly, genetic ablation of PPARγ in ILC2s significantly suppresses tumor growth in vivo. Our findings highlight a crucial role for PPARγ in supporting the IL-33 dependent pro-tumorigenic role of ILC2s and suggest that PPARγ can be considered as a druggable pathway in ILC2s to inhibit their effector functions. Hence, PPARγ targeting might be exploited in cancer immunotherapy and in other ILC2-driven mediated disorders, such as asthma and allergy.
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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.