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We began analyzing https://www.nature.com/articles/s42003-024-05922-2, but it redirected us to https://www.nature.com/articles/s42003-024-05922-2. The analysis below is for the second page.

Title[redir]:
Decreased progenitor TCF1 + T-cells correlate with COVID-19 disease severity | Communications Biology
Description:
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. This study shows that severity of disease in COVID-19 patients is characterized by the preferential loss of TCF1+ progenitor T-cells needed to self-renew and replenish the immune system.

Matching Content Categories {📚}

  • Science
  • Education
  • Health & Fitness

Content Management System {📝}

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Custom-built

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Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {🔍}

tcf, expression, severe, tcells, patients, cells, disease, pubmed, fig, article, mild, covid, cell, google, scholar, cas, analysis, loss, central, severity, healthy, donors, subsets, cases, lower, panel, observed, clusters, supplementary, reduced, peripheral, reduction, samples, increase, nodes, cluster, presence, effector, decrease, memory, data, showed, blood, levels, decline, upper, caspase, histogram, spade, tree,

Topics {✒️}

nature portfolio est-de-l'île-de-montréal apc-conjugated anti-tcr alpha/beta privacy policy {{{{\backslash }}}}[{{{{{\rm{cpa}}}}}}-{{{{{\rm{cemtl\backslash }}}}}}] fitc-conjugated anti-tcr gamma/delta thermo fisher scientific granulocyte-macrophage colony-stimulating factor c-jun n-terminal kinase cd8+ subset cd38 + hla-dr+ki67+12 advertising apc-cy7-conjugated anti-cd69 pe-cf594-conjugated anti-granzyme anti-tcr gamma/delta antibodies long-lasting pro-survival signals60 research blood collection human research participants research institute researcher reprints nature 587 nature 595 nature 476 nature 537 nature 571 nature research design lower middle panel author information authors step real-time rt-pcr cd8 + t-cells expressing granzyme tcf1 + versus tcf1- t-cells cysteine-aspartic acid protease cytotoxic sars-cov-2-reactive cd4 cd3 + cd8+ peripheral t-cells af700-conjugated anti-cd3 pe-conjugated anti-tcf1 fitc-conjugated anti-ki67 bv785-conjugated anti-cd8 real-time pcr assay68 real-time pcr amplification bv605-conjugated anti-pd-1 {{{{\backslash }}}}[{{{{{\rm{iqr\backslash }}}}}}] involve pro-inflammatory interleukins middle panel pecy7-conjugated anti-ifng buv395-conjugated anti-cd4 lymphoid enhancer-binding factor-1 tcr-beta + t-cells cd3 + cd4-cd8- t-cells

Schema {🗺️}

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         headline:Decreased progenitor TCF1 + T-cells correlate with COVID-19 disease severity
         description: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. This study shows that severity of disease in COVID-19 patients is characterized by the preferential loss of TCF1+ progenitor T-cells needed to self-renew and replenish the immune system.
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      headline:Decreased progenitor TCF1 + T-cells correlate with COVID-19 disease severity
      description: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. This study shows that severity of disease in COVID-19 patients is characterized by the preferential loss of TCF1+ progenitor T-cells needed to self-renew and replenish the immune system.
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