ArticleNature immunology2024
GPR34 is a metabolic immune checkpoint for ILC1-mediated antitumor immunity.
Article in Nature immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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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
18 citing papers in PubMed.
- LysoPS-GPR34 axis enhances tumor-associated macrophages efferocytosis to promote immune escape in gastric cancer peritoneal metastasis.Journal for immunotherapy of cancer · 2026Article
- Identification of macrophage-enriched genes in ovarian cancer by single-cell RNA sequencing and establishment of a prognosis model.Scientific reports · 2026Article
- Fatty Acid Metabolism in Health and Cancer: From Fundamental Mechanisms to Therapeutic Application.MedComm · 2026Review
- Lipid metabolism reprogramming shapes the immune landscape in the tumor microenvironment.Cellular & molecular immunology · 2026Review
- Targeting GPR34 in damage-associated macrophages enhances anti-tumor immunity and the efficacy of Surufatinib in pancreatic cancer.Signal transduction and targeted therapy · 2026Article
- Tumor microenvironment-driven natural killer cell diversity: mechanisms and therapeutic opportunities.Cancer biology & medicine · 2026Review
- Nerves Stimulate Cross-talk Between Gastric Cancer and Group 3 Innate Lymphoid Cells to Enhance Immunosuppression.Cancer research · 2026Article
- Impaired removal of dying brain cells by microglia in Gpr34 deficient mice.Journal of neuroinflammation · 2026Article
- Splenic cDC1 efferocytosis and cross-presentation to CD8 T cells are promoted by GPR34 and lysophosphatidylserine.The Journal of experimental medicine · 2026Article
- An Interpretable Omics-to-Image Transformer Framework for Cancer Prognosis Prediction.Computational and structural biotechnology journal · 2026Article
- GPR34 inhibition reprograms tumor-associated macrophages and enhances the sensitivity of anti-PD-1 therapy in hepatocellular carcinoma.Cancer cell international · 2025Article
- Immunometabolism: crosstalk with tumor metabolism and implications for cancer immunotherapy.Molecular cancer · 2025Review
- Progress in the Application of Marine Polysaccharide Drug Delivery Systems in Tumor Immunotherapy: Multiple Mechanisms and Material Forms.Marine drugs · 2025Review
- Dissecting the heterogeneity and tumor-associated dynamics of human liver group I ILC via scRNA sequencing data.Immunologic research · 2025Article
- Innate Lymphoid Cells Are the Rheostat of Immune Response in the Kidney.Journal of cellular and molecular medicine · 2025Review
- Spatial profiling of the metabolism-immune axis in ovarian cancer.Frontiers in pharmacology · 2025Review
- Innate lymphoid cells in the spotlight: from biomarkers to blueprint for innovative immunotherapy.Frontiers in immunology · 2025Review
- The advantages of NK cell vaccines in solid carcinoma clinical trials: conducted by various biology strategy and technology.Frontiers in medicine · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
Abstract
Type 1 innate lymphoid cells (ILC1s) are a class of tissue-resident cells with antitumor activity, suggesting its possible role in solid tumor immune surveillance, but it is not clear whether manipulating ILC1s can induce potent antitumor immune responses. Here, we found that G-protein-coupled receptor 34 (GPR34), a receptor for lysophosphatidylserine (LysoPS), was highly expressed on ILC1s but not on conventional natural killer cells in the tumor microenvironment. LysoPS was enriched in the tumor microenvironment and could inhibit ILC1 activation via GPR34. Genetic deletion of LysoPS synthase Abhd16a expression in tumors or Gpr34 expression in ILC1s or antagonizing GPR34 enhanced ILC1 antitumor activity. In individuals with cancer, ABHD16A expression in tumors or GPR34 expression in ILC1s was inversely correlated with the antitumor activity of ILC1s or ILC1-like cells. Thus, our results demonstrate that manipulating ILC1s can induce potent antitumor immunity, and GPR34 is a metabolic immune checkpoint that can be targeted to develop ILC1-based immunotherapy.
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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.