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- Title
Delayed generation of functional virus-specific circulating T follicular helper cells correlates with severe COVID-19.
- Authors
Yu, Meng; Charles, Afandi; Cagigi, Alberto; Christ, Wanda; Österberg, Björn; Falck-Jones, Sara; Azizmohammadi, Lida; Åhlberg, Eric; Falck-Jones, Ryan; Svensson, Julia; Nie, Mu; Warnqvist, Anna; Hellgren, Fredrika; Lenart, Klara; Arcoverde Cerveira, Rodrigo; Ols, Sebastian; Lindgren, Gustaf; Lin, Ang; Maecker, Holden; Bell, Max
- Abstract
Effective humoral immune responses require well-orchestrated B and T follicular helper (Tfh) cell interactions. Whether these interactions are impaired and associated with COVID-19 disease severity is unclear. Here, longitudinal blood samples across COVID-19 disease severity are analysed. We find that during acute infection SARS-CoV-2-specific circulating Tfh (cTfh) cells expand with disease severity. SARS-CoV-2-specific cTfh cell frequencies correlate with plasmablast frequencies and SARS-CoV-2 antibody titers, avidity and neutralization. Furthermore, cTfh cells but not other memory CD4 T cells, from severe patients better induce plasmablast differentiation and antibody production compared to cTfh cells from mild patients. However, virus-specific cTfh cell development is delayed in patients that display or later develop severe disease compared to those with mild disease, which correlates with delayed induction of high-avidity neutralizing antibodies. Our study suggests that impaired generation of functional virus-specific cTfh cells delays high-quality antibody production at an early stage, potentially enabling progression to severe disease. T follicular helper cells (Tfh) enhance antibody responses and can circulate or be resident in lymph nodes. Here the authors show that during acute SARS-CoV-2 infection, circulating Tfh cells correlate with antibody titres and plasmablast levels but in more severe COVID-19 cases, cTfh generation is delayed.
- Subjects
T helper cells; IMMUNOLOGIC memory; COVID-19; ANTIBODY formation; COVID-19 pandemic; ANTIBODY titer
- Publication
Nature Communications, 2023, Vol 14, Issue 1, p1
- ISSN
2041-1723
- Publication type
Article
- DOI
10.1038/s41467-023-37835-9