dc.contributor.author | Tu, Thai Hien | |
dc.contributor.author | Grunbaum, Ami | |
dc.contributor.author | François, Santinon | |
dc.contributor.author | Kazanova, Alexandra | |
dc.contributor.author | Rozza, Nicholas | |
dc.contributor.author | Kremer, Richard | |
dc.contributor.author | Mihalcioiu, Catalin | |
dc.contributor.author | Rudd, Christopher E. | |
dc.date.accessioned | 2024-06-03T11:51:23Z | |
dc.date.available | NO_RESTRICTION | fr |
dc.date.available | 2024-06-03T11:51:23Z | |
dc.date.issued | 2024-05-03 | |
dc.identifier.uri | http://hdl.handle.net/1866/33301 | |
dc.publisher | Nature research | fr |
dc.rights | Ce document est mis à disposition selon les termes de la Licence Creative Commons
Attribution - Pas d’utilisation commerciale 4.0 International. / This work is licensed under a
Creative Commons Attribution - NonCommercial 4.0 International License. | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/deed.fr | |
dc.title | Decreased progenitor TCF1 + T-cells correlate with COVID-19 disease severity | fr |
dc.type | Article | fr |
dc.contributor.affiliation | Université de Montréal. Faculté de médecine. Département de médecine | fr |
dc.identifier.doi | 10.1038/s42003-024-05922-2 | |
dcterms.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. | fr |
dcterms.isPartOf | urn:ISSN: 2399-3642 | fr |
dcterms.language | eng | fr |
UdeM.ReferenceFournieParDeposant | 10.1038/s42003-024-05922-2 | fr |
UdeM.VersionRioxx | Version publiée / Version of Record | fr |
oaire.citationTitle | Communications biology | fr |
oaire.citationVolume | 7 | fr |