ReviewFrontiers in immunology2026
The lactylation-immunosuppression network in cancer: driving a metabolic-epigenetic axis.
Review in Frontiers in immunology, 2026. 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.
- Lactylation Remodels Tumorigenesis, Immune Microenvironment, and Therapeutic Response.Current issues in molecular biology · 2026Review
- The Dynamic Alliance of p53 and Metabolism in the Tumor Microenvironment Shapes Tumor Evolution.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Review
- Metabolic-epigenetic crosstalk in latent autoimmune diabetes in adults: potential roles of lactate-induced histone lactylation in immune regulation and pancreatic β-cell fate.Frontiers in endocrinology · 2026Review
- The symbiotic axis between the acidic tumor microenvironment and cancer stem cells: a driver of malignancy and therapeutic resistance.Frontiers in oncology · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
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Abstract
The accumulation of lactate in the tumor microenvironment (TME), driven by the Warburg effect, is closely associated with immunosuppression. Lactate can contribute to this process through lysine lactylation, a novel post-translational modification. We propose a conceptual framework, the "Lactylation-immunosuppression network," that links tumor metabolic reprogramming to immune cell signaling and gene expression. This network highlights a metabolic-epigenetic axis linking lactylation to immunosuppression via a synergistic dual mechanism: long-term epigenetic programming via histone lactylation establishes a stable immunosuppressive transcriptome, while rapid, dynamic non-histone lactylation directly modulates protein activity and stability, thereby potentiating function. This review summarizes how lactylation may undermine anti-tumor immunity by remodeling myeloid and T cell compartments, fortifying immune checkpoint barriers, and creating self-reinforcing metabolic feedback loops. By elucidating this mechanism, we highlight novel therapeutic targets, propose a "kinetic threshold" model to resolve the paradoxical role of lactate, and provide a unified conceptual framework for developing next-generation immunotherapies and guiding future mechanistic studies.
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Registered trials
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