ArticleFrontiers in immunology2025
Histone lactylation-derived TET2 enhanced Arg1-mediated MDSC immunosuppression.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Epigenetic pacemaker: A review of DNA methylation, histone lactylation, and non-coding RNAs in autoimmune skin diseases.Journal of translational autoimmunity · 2026Review
- Lactylation Remodels Tumorigenesis, Immune Microenvironment, and Therapeutic Response.Current issues in molecular biology · 2026Review
- CD55-expressing myeloid-derived suppressor cells (MDSCs) drive cancer immunoevasion.Journal for immunotherapy of cancer · 2026Article
- Lactylation: a novel epigenetic bridge connecting metabolic reprogramming and immune dysregulation in sepsis-associated ARDS.Frontiers in immunology · 2026Review
- The lactylation axis: bridging metabolic reprogramming and immunosuppression in the tumor microenvironment.Frontiers in immunology · 2026Review
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Authors and funding
9 authors.
Funding
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Abstract
In the tumor microenvironment (TME), tumor cells secrete a large amounts of lactate due to the "Warburg effect", which plays a significant role in regulating gene transcription. Recently, the role of lactate in gene transcription has been increasingly understood. Myeloid-derived suppressor cells (MDSCs) are inhibitory cells of bone marrow origin that possess marked abilities to suppress immune cell responses. Within the TME, MDSCs inhibit T cell-mediated specific anti-tumor immunity, as well as non-specific anti-tumor immunity mediated by NK cells and macrophages, by expressing high levels of Arg1, iNOS, and ROS. Methods: This study used the Lewis lung carcinoma cell line to establish a lung cancer xenograft model; MDSCs were isolated from the spleens of these mice for subsequent experiments. Protein expression was analyzed by Western blotting, mRNA expression by qRT-PCR, protein-DNA interactions by ChIP-qPCR, and DNA methylation by MSP-qPCR. Result: This research shows that histone lactylation enhances the immunosuppressive function of MDSCs. Mechanistically, lactate-induced histone lactylation upregulates TET2, which, using STAT3 as a bridge, modulates ARG1 promoter methylation to upregulate its expression and ultimately enhance the immunosuppressive function of MDSCs. Conclusion: This research reveals that the histone lactylation-mediated alteration of TET2 presents a novel therapeutic target for cancer treatment.
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