The DOI matches its Crossref record; 226 of the 226 references it cites were found in a registry or an index.
Lactate: A key regulator of the immune response
Open accessAbstract
Lactate, the end product of both anaerobic and aerobic glycolysis in proliferating and growing cells-with the latter process known as the Warburg effect-is historically considered a mere waste product of cell and tissue metabolism. However, research over the past ten years has unveiled multifaceted functions of lactate that critically shape and impact cellular biology. Beyond serving as a fuel source, lactate is now known to influence gene expression through histone modification and to function as a signaling molecule that impacts a wide range of cellular activities. These properties have been particularly studied in the context of both adaptive and innate immune responses. Here, we review the diverse roles of lactate in the regulation of the immune system during homeostasis and disease pathogenesis (including cancer, infection, cardiovascular diseases, and autoimmunity). Furthermore, we describe recently proposed therapeutic interventions for manipulating lactate metabolism in human diseases.
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Cites
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Metabolic regulation of gene expression by histone lactylation
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Functional Polarization of Tumour-Associated Macrophages by Tumour-Derived Lactic Acid
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Posttranscriptional Control of T Cell Effector Function by Aerobic Glycolysis
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LDHA-Associated Lactic Acid Production Blunts Tumor Immunosurveillance by T and NK Cells
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Glucose feeds the TCA cycle via circulating lactate
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Metadata
- Authors
- Llibre, A., Kucuk, S., Gope, A., Certo, M., & Mauro, C.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2025-03
- Volume
- 58
- Issue
- 3
- Pages
- 535-554
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W4408310291
- Cited by
- 283
- References
- 226
- FWCI
- 93.37
- Type
- journal article
- Language
- en
- Open access
- hybrid
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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