Single-cell transcriptomic analysis of SARS-CoV-2 reactive CD4<sup>+</sup>T cells

Meckiff, Benjamin J, Ramírez-Suástegui, Ciro, Fajardo, Vicente, Chee, Serena J, Kusnadi, Anthony, Simon, Hayley, Grifoni, Alba, Pelosi, Emanuela, Weiskopf, Daniela, Sette, Alessandro
et al (show 4 more authors) (2020) Single-cell transcriptomic analysis of SARS-CoV-2 reactive CD4<sup>+</sup>T cells. Cell.

Access the full-text of this item by clicking on the Open Access link.


<jats:title>ABSTRACT</jats:title><jats:p>The contribution of CD4<jats:sup>+</jats:sup>T cells to protective or pathogenic immune responses to SARS-CoV-2 infection remains unknown. Here, we present large-scale single-cell transcriptomic analysis of viral antigen-reactive CD4<jats:sup>+</jats:sup>T cells from 32 COVID-19 patients. In patients with severe disease compared to mild disease, we found increased proportions of cytotoxic follicular helper (T<jats:sub>FH</jats:sub>) cells and cytotoxic T helper cells (CD4-CTLs) responding to SARS-CoV-2, and reduced proportion of SARS-CoV-2 reactive regulatory T cells. Importantly, the CD4-CTLs were highly enriched for the expression of transcripts encoding chemokines that are involved in the recruitment of myeloid cells and dendritic cells to the sites of viral infection. Polyfunctional T helper (T<jats:sub>H</jats:sub>)1 cells and T<jats:sub>H</jats:sub>17 cell subsets were underrepresented in the repertoire of SARS-CoV-2-reactive CD4<jats:sup>+</jats:sup>T cells compared to influenza-reactive CD4<jats:sup>+</jats:sup>T cells. Together, our analyses provide so far unprecedented insights into the gene expression patterns of SARS-CoV-2 reactive CD4<jats:sup>+</jats:sup>T cells in distinct disease severities.</jats:p>

Item Type: Article
Divisions: Faculty of Health and Life Sciences
Faculty of Health and Life Sciences > Institute of Systems, Molecular and Integrative Biology
Depositing User: Symplectic Admin
Date Deposited: 23 Dec 2021 08:02
Last Modified: 18 Jan 2023 21:18
DOI: 10.1101/2020.06.12.148916
Open Access URL:
Related URLs: