Type I Interferon Autoantibodies Correlate With Cellular Immune Alterations in Severe COVID-19

The Karolinska KI/K COVID-19 Study Group, Benedikt Strunz, Christopher Maucourant, Adi Mehta, Hui Wan, Likun Du, Dan Sun, Puran Chen, Anna Nordlander, Yu Gao, Martin Cornillet, Jonna Bister, Egle Kvedaraite, Wanda Christ, Jonas Klingström, Daniel Geanon, Åsa Parke, Anna Ekwall-Larson, Laura Rivino, Paul A MacArySoo Aleman, Marcus Buggert, Hans-Gustaf Ljunggren, Qiang Pan-Hammarström, Fridtjof Lund-Johansen, Kristoffer Strålin, Niklas K Björkström*

*Corresponding author for this work

Research output: Contribution to journalArticle (Academic Journal)peer-review

Abstract

Background:
Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can lead to severe disease with increased morbidity and mortality among certain risk groups. The presence of autoantibodies against type I interferons (aIFN-Abs) is one mechanism that contributes to severe coronavirus disease 2019 (COVID-19).

Methods:
This study aimed to investigate the presence of aIFN-Abs in relation to the soluble proteome, circulating immune cell numbers, and cellular phenotypes, as well as development of adaptive immunity.

Results:
aIFN-Abs were more prevalent in critical compared to severe COVID-19 but largely absent in the other viral and bacterial infections studied here. The antibody and T-cell response to SARS-CoV-2 remained largely unaffected by the presence aIFN-Abs. Similarly, the inflammatory response in COVID-19 was comparable in individuals with and without aIFN-Abs. Instead, presence of aIFN-Abs had an impact on cellular immune system composition and skewing of cellular immune pathways.

Conclusions:
Our data suggest that aIFN-Abs do not significantly influence development of adaptive immunity but covary with alterations in immune cell numbers.
Original languageEnglish
Article numberjiae036
Pages (from-to)e318-e326
Number of pages10
JournalThe Journal of infectious diseases
Volume230
Issue number2
Early online date29 Feb 2024
DOIs
Publication statusPublished - 15 Aug 2024

Bibliographical note

Publisher Copyright:
© The Author(s) 2024. Published by Oxford University Press on behalf of Infectious Diseases Society of America.

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