Type I Interferon Autoantibodies Correlate With Cellular Immune Alterations in Severe COVID-19.
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Strunz B, Maucourant C, Mehta A, Wan H, Du L, Sun D, Chen P, Nordlander A, Gao Y, Cornillet M, Bister J, Kvedaraite E, Christ W, Klingström J, Geanon D, Parke Å, Ekwall-Larson A, Rivino L, MacAry PA, Aleman S, Buggert M, Ljunggren H, Pan-Hammarström Q, Lund-Johansen F, Strålin K, Björkström NK, Group KKCS, ,
The Journal of Infectious Diseases - (-) - [2024-02-29; online 2024-02-29]
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). 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. 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. Our data suggest that aIFN-Abs do not significantly influence development of adaptive immunity but covary with alterations in immune cell numbers.
Funder: KAW/SciLifeLab National COVID program
PubMed 38421006
DOI 10.1093/infdis/jiae036
Crossref 10.1093/infdis/jiae036
pii: 7616238