ArticleClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2024
Glycolysis: An early marker for vancomycin-specific T-cell activation.
Article in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 3 citations in OpenAlex.
- Metabolic impairments in peripheral blood mononuclear cells after BNT162b2 vaccination in liver transplantation adolescents.Scientific reports · 2026Article
- Elucidating CD4+ and CD8+ T-cell involvement in patients with vancomycin-induced DRESS.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Glycolysis: An early marker for vancomycin-specific T-cell activation.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2024Article
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Authors and funding
11 authors at 6 institutions in 4 countries.
Funding
Abstract
backgroundVancomycin, a glycopeptide antibiotic used for Gram-positive bacterial infections, has been linked with drug reaction with eosinophilia and systemic symptoms (DRESS) in HLA-A*32:01-expressing individuals. This is associated with activation of T lymphocytes, for which glycolysis has been isolated as a fuel pathway following antigenic stimulation. However, the metabolic processes that underpin drug-reactive T-cell activation are currently undefined and may shed light on the energetic conditions needed for the elicitation of drug hypersensitivity or tolerogenic pathways. Here, we sought to characterise the immunological and metabolic pathways involved in drug-specific T-cell activation within the context of DRESS pathogenesis using vancomycin as model compound and drug-reactive T-cell clones (TCCs) generated from healthy donors and vancomycin-hypersensitive patients.
methodsCD4+ and CD8+ vancomycin-responsive TCCs were generated by serial dilution. The Seahorse XFe
resultsModel T-cell stimulants induced non-specific T-cell activation, characterised by immediate augmentation of ECAR and rate of ATP production (JATPglyc). There was a dose-dependent and drug-specific glycolytic shift when vancomycin-reactive TCCs were exposed to the drug. Vancomycin-reactive TCCs did not exhibit T-cell cross-reactivity with structurally similar compounds within proliferative and cytokine readouts. However, cross-reactivity was observed when analysing energetic responses; TCCs with prior specificity for vancomycin were also found to exhibit glycolytic switching after exposure to teicoplanin. Glycolytic activation of TCC was HLA restricted, as exposure to HLA blockade attenuated the glycolytic induction.
conclusionThese studies describe the glycolytic shift of CD4+ and CD8+ T cells following vancomycin exposure. Since similar glycolytic switching is observed with teicoplanin, which did not activate T cells, it is possible the master switch for T-cell activation is located upstream of metabolic signalling.
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