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  3. Persistent immune abnormalities discriminate post-COVID syndrome from convalescence
 

Persistent immune abnormalities discriminate post-COVID syndrome from convalescence

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BORIS DOI
10.48620/88280
Publisher DOI
10.1007/s15010-023-02164-y
Description
Background: Innate lymphoid cells (ILCs) are key organizers of tissue immune responses and regulate tissue development, repair, and pathology. Persistent clinical sequelae beyond 12 weeks following acute COVID-19 disease, named post-COVID syndrome (PCS), are increasingly recognized in convalescent individuals. ILCs have been associated with the severity of COVID-19 symptoms but their role in the development of PCS remains poorly defined.

Methods and results: Here, we used multiparametric immune phenotyping, finding expanded circulating ILC precursors (ILCPs) and concurrent decreased group 2 innate lymphoid cells (ILC2s) in PCS patients compared to well-matched convalescent control groups at > 3 months after infection or healthy controls. Patients with PCS showed elevated expression of chemokines and cytokines associated with trafficking of immune cells (CCL19/MIP-3b, FLT3-ligand), endothelial inflammation and repair (CXCL1, EGF, RANTES, IL-1RA, PDGF-AA).

Conclusion: These results define immunological parameters associated with PCS and might help find biomarkers and disease-relevant therapeutic strategies.
Date of Publication
2024-02-07
Publication Type
Article
Language(s)
en
Contributor(s)
Sbierski-Kind, Julia
Schlickeiser, Stephan
Feldmann, Svenja
Ober, Veronica
Grüner, Eva
Pleimelding, Claire
Gilberg, Leonard
Brand, Isabel
Weigl, Nikolas
Ahmed, Mohamed I. M.
Ibarra, Gerardo
Ruzicka, Michael
Benesch, Christopher
Pernpruner, Anna
Valdinoci, Elisabeth
Hoelscher, Michael
Adorjan, Kristina
Stubbe, Hans Christian
Pritsch, Michael
Seybold, Ulrich
Roider, Julia
Additional Credits
University Hospital of Psychiatry and Psychotherapy
Zentrum für Translationale Forschung der Universitätsklinik für Psychiatrie und Psychotherapie
Series
Infection
Publisher
Springer
ISSN
0300-8126
1439-0973
Access(Rights)
open.access
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