ArticleCellular and molecular life sciences : CMLS2023
Myeloid-derived suppressor cells impair CD4+ T cell responses during chronic Staphylococcus aureus infection via lactate metabolism.
Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Research progress on T-cell responses inFrontiers in microbiology · 2026Pooled it
- Reversing Macrophage Immunometabolic Dysfunction in Prolonged Infections Via a Glutaminolysis-Fueled Restoration-Based Hierarchically Selective Therapeutic System.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Myeloid-Derived Suppressor Cells in Cancer: Metabolic Reprogramming, Immune Crosstalk, and Therapeutic Targeting.Cancers · 2026Review
- Mitochondrial transfer to granulocytic myeloid-derived suppressor cells augments immunosuppressive activity.Cell reports · 2026Article
- Rational Combination of Dominant and Subdominant Antigens with Nanoadjuvant Elicits Durable Immunity AgainstVaccines · 2026Article
- uPAR expression in M-MDSCs under high LDHA activity in pancreatic ductal adenocarcinoma.Scientific reports · 2025Article
- Targeting pyruvate metabolism generates distinct CD8+ T cell responses to gammaherpesvirus and B lymphoma.JCI insight · 2025Article
- A new method to measure cell metabolism of rare cells in vivo reveals a high oxidative phosphorylation dependence of lung T cells.Immunology and cell biology · 2025Article
- ANXA2 in cancer: aberrant regulation of tumour cell apoptosis and its immune interactions.Cell death discovery · 2025Review
- Tumor metabolic regulators: key drivers of metabolic reprogramming and the promising targets in cancer therapy.Molecular cancer · 2025Review
- Pharmacological and genetic inhibition of ARG2 in CXCR2Theranostics · 2025Article
- Endoplasmic reticulum stress orchestrates tumor metabolism and immunity: new insights into immunometabolic therapeutics.Frontiers in immunology · 2025Review
- Exploring the Potential of Glycolytic Modulation in Myeloid-Derived Suppressor Cells for Immunotherapy and Disease Management.Immune network · 2024Review
- Mechanisms underlying immunosuppression by regulatory cells.Frontiers in immunology · 2024Review
- Nitric oxide-producing monocyte-myeloid suppressor cells expand and accumulate in the spleen and mesenteric lymph nodes ofFrontiers in cellular and infection microbiology · 2024Article
- Metabolic pathways fueling the suppressive activity of myeloid-derived suppressor cells.Frontiers in immunology · 2024Review
- Glycolysis in the tumor microenvironment: a driver of cancer progression and a promising therapeutic target.Frontiers in cell and developmental biology · 2024Review
- Engaging natural regulatory myeloid cells to restrict T-cell hyperactivation-induced liver inflammation via extracellular vesicle-mediated purine metabolism regulation.Theranostics · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Staphylococcus aureus is an important cause of chronic infections resulting from the failure of the host to eliminate the pathogen. Effective S. aureus clearance requires CD4+ T cell-mediated immunity. We previously showed that myeloid-derived suppressor cells (MDSC) expand during staphylococcal infections and support infection chronicity by inhibiting CD4+ T cell responses. The aim of this study was to elucidate the mechanisms underlying the suppressive effect exerted by MDSC on CD4+ T cells during chronic S. aureus infection. It is well known that activated CD4+ T cells undergo metabolic reprogramming from oxidative metabolism to aerobic glycolysis to meet their increased bioenergetic requirements. In this process, pyruvate is largely transformed into lactate by lactate dehydrogenase with the concomitant regeneration of NAD+, which is necessary for continued glycolysis. The by-product lactate needs to be excreted to maintain the glycolytic flux. Using SCENITH (single-cell energetic metabolism by profiling translation inhibition), we demonstrated here that MDSC inhibit CD4+ T cell responses by interfering with their metabolic activity. MDSC are highly glycolytic and excrete large amount of lactate in the local environment that alters the transmembrane concentration gradient and prevent removal of lactate by activated CD4+ T. Accumulation of endogenous lactate impedes the regeneration of NAD+, inhibit NAD-dependent glycolytic enzymes and stop glycolysis. Together, the results of this study have uncovered a role for metabolism on MDSC suppression of CD4+ T cell responses. Thus, reestablishment of their metabolic activity may represent a mean to improve the functionality of CD4+ T cells during chronic S. aureus infection.
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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.