ArticleThe Journal of clinical investigation2021
Metabolic imbalance of T cells in COVID-19 is hallmarked by basigin and mitigated by dexamethasone.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 34 citations in OpenAlex.
- Meplazumab in hospitalized adults with severe COVID-19 (DEFLECT): a multicenter, seamless phase 2/3, randomized, third-party double-blind clinical trial.Signal transduction and targeted therapy · 2023Trial
- Metabolic immune checkpoints (MICs) in cancer: from molecular mechanisms to challenges and opportunities in clinical translation.Signal transduction and targeted therapy · 2026Review
- A late-stage multi-dimensional intervention rescues lethal viral pneumonia in an aged hamster model.Molecular biomedicine · 2026Article
- Cognition-Linked Monocyte State Reveals Altered Myeloid-Lymphoid Coordination in Neuro-PASC.International journal of molecular sciences · 2026Article
- Post-COVID impairment of T cell responses to community-acquired pathogens can be modified by activating cellular metabolism.PLoS pathogens · 2026Article
- Post-COVID impairment of memory T cell responses to community-acquired pathogens can be rectified by activating cellular metabolism.bioRxiv : the preprint server for biology · 2026Article
- Increased expression of CD36 and CD163 in clear cell renal cell carcinoma suggests an association between lipid transport and an "M2-like" macrophage phenotype.Frontiers in immunology · 2026Article
- Mitochondrial function is impaired in long COVID patients.Annals of medicine · 2025Observational
- COVID-19-associated Autoimmune and Inflammatory Diseases: Molecular Mechanisms and the Role of IVIG Therapy.Clinical reviews in allergy & immunology · 2025Review
- Cyclophilin-CD147 interaction enables SARS-CoV-2 infection of human monocytes and their activation via Toll-like receptors 7 and 8.Frontiers in immunology · 2025Article
- T-cell exhaustion in COVID-19: what do we know?Frontiers in immunology · 2025Review
- The effects of CypA on apoptosis: potential target for the treatment of diseases.Applied microbiology and biotechnology · 2024Review
- Glucocorticoid therapy for acute respiratory distress syndrome: Current concepts.Journal of intensive medicine · 2024Review
- Impacts of cryopreservation on phenotype and functionality of mononuclear cells in peripheral blood and ascites.Journal of translational internal medicine · 2024Article
- Metabolic dysregulation impairs lymphocyte function during severe SARS-CoV-2 infection.Communications biology · 2023Article
- A multi-omics based anti-inflammatory immune signature characterizes long COVID-19 syndrome.iScience · 2023Article
- The retina-specific basigin isoform does not induce IL-6 expression in mouse monocytes.Molecular vision · 2023Article
- Tracking the clonal dynamics of SARS-CoV-2-specific T cells in children and adults with mild/asymptomatic COVID-19.Clinical immunology (Orlando, Fla.) · 2023Article
- Proinflammatory Innate Cytokines and Distinct Metabolomic Signatures Shape the T Cell Response in Active COVID-19.Vaccines · 2022Article
- Renaissance of glucocorticoids in critical care in the era of COVID-19: ten urging questions.Critical care (London, England) · 2022Review
Corrections and comments
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Authors and funding
46 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic pathways regulate immune responses and disrupted metabolism leads to immune dysfunction and disease. Coronavirus disease 2019 (COVID-19) is driven by imbalanced immune responses, yet the role of immunometabolism in COVID-19 pathogenesis remains unclear. By investigating 87 patients with confirmed SARS-CoV-2 infection, 6 critically ill non-COVID-19 patients, and 47 uninfected controls, we found an immunometabolic dysregulation in patients with progressed COVID-19. Specifically, T cells, monocytes, and granulocytes exhibited increased mitochondrial mass, yet only T cells accumulated intracellular reactive oxygen species (ROS), were metabolically quiescent, and showed a disrupted mitochondrial architecture. During recovery, T cell ROS decreased to match the uninfected controls. Transcriptionally, T cells from severe/critical COVID-19 patients showed an induction of ROS-responsive genes as well as genes related to mitochondrial function and the basigin network. Basigin (CD147) ligands cyclophilin A and the SARS-CoV-2 spike protein triggered ROS production in T cells in vitro. In line with this, only PCR-positive patients showed increased ROS levels. Dexamethasone treatment resulted in a downregulation of ROS in vitro and T cells from dexamethasone-treated patients exhibited low ROS and basigin levels. This was reflected by changes in the transcriptional landscape. Our findings provide evidence of an immunometabolic dysregulation in COVID-19 that can be mitigated by dexamethasone treatment.
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