ArticleCommunications biology2024
Decreased progenitor TCF1 + T-cells correlate with COVID-19 disease severity.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- GSK-3 regulates CD4-CD8 cooperation for super-armed CD8+ cytolytic T cells in immunotherapy against tumors.Signal transduction and targeted therapy · 2026Article
- Accurate profiling of single-cell alternative transcript start sites by correcting RNA degradation.Nature communications · 2026Article
- An explainable prognostic model after vascularized bone grafting for hip preservation based on CT radiomics combined with SHAP.Physical and engineering sciences in medicine · 2026Article
- Imbalanced immune cell network and suboptimal cell activation: signatures associated with disease severity in vaccine-naïve COVID-19 patients.Frontiers in immunology · 2026Article
- Fgl2 regulates FcγRIIB+CD8+ T cell responses during infection.JCI insight · 2025Article
- The identification of a SARs-CoV2 S2 protein derived peptide with super-antigen-like stimulatory properties on T-cells.Communications biology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
COVID-19, caused by SARS-CoV-2, can lead to a severe inflammatory disease characterized by significant lymphopenia. However, the underlying cause for the depletion of T-cells in COVID-19 patients remains incompletely understood. In this study, we assessed the presence of different T-cell subsets in the progression of COVID-19 from mild to severe disease, with a focus on TCF1 expressing progenitor T-cells that are needed to replenish peripheral T-cells during infection. Our results showed a preferential decline in TCF1+ progenitor CD4 and CD8+ T-cells with disease severity. This decline was seen in various TCF1+ subsets including naive, memory and effector-memory cells, and surprisingly, was accompanied by a loss in cell division as seen by a marked decline in Ki67 expression. In addition, TCF1+ T-cells showed a reduction in pro-survival regulator, BcL2, and the appearance of a new population of TCF1 negative caspase-3 expressing cells in peripheral blood from patients with severe disease. The decline in TCF1+ T-cells was also seen in a subgroup of severe patients with vitamin D deficiency. Lastly, we found that sera from severe patients inhibited TCF1 transcription ex vivo which was attenuated by a blocking antibody against the cytokine, interleukin-12 (IL12). Collectively, our findings underscore the potential significance of TCF1+ progenitor T-cells in accounting for the loss of immunity in severe COVID-19 and outline an array of markers that could be used to identify disease progression.
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