ArticleNature communications2025
Metabotropic glutamate receptor 4-mediated glutamatfergic signaling reshapes the tumor microenvironment by regulating dendritic cell maturation.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Neural regulation of cancer: from synaptic integration to neuro-immune regulation.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- The Glutamate-Glutathione axis in neuropsychiatric disorders and cancer: From shared mechanisms to non-invasive biomarkers.Redox biology · 2026Review
- Fungal metabolite-based immunotherapy overcomes tumor-associated macrophage immunosuppression.Cell reports. Medicine · 2026Article
- Perforin-2 enhances antigen-specific CTL immune response by promoting cross presentation.Cell death & disease · 2026Article
- Role of the neurotransmitter-receptor pathway in T-cell tumor immunology and cancer immunotherapy.Acta biochimica et biophysica Sinica · 2026Review
- Metabolic reprogramming and immune evasion interaction in the tumor microenvironment promote tumor progression.Frontiers in oncology · 2026Review
- Slc1a2-mediated Glutamate Transport Promotes Dendritic Cell Immunity through Sema3A-regulated Cytoskeletal Remodeling and Migration.International journal of biological sciences · 2026Article
- Neurotransmitters as regulators of autoimmunity: mechanisms and translational targeting.NPJ autoimmunity · 2026Review
- Modulating glutamate neurotransmission inFrontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabotropic glutamate receptor 4 (mGluR4, encoded by Grm4), is a neurotransmitter receptor, known to play roles in tumor progression and immune modulation through the nervous system. Here we show that mGluR4 may regulate immune responses in the tumor microenvironment (TME) also via non-neuronal mechanisms. We observe that dendritic cells (DC) from mGluR4-deficient mice display enhanced migration, maturation and antigen-presentation capacity, which promote T cell and NK cell responses against tumor cells. Tumor growth and metastases are suppressed in Grm4
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Registered trials
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