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Journal Article

IL-33 expression in response to SARS-CoV-2 correlates with seropositivity in COVID-19 convalescent individuals

MPS-Authors

Stanczak,  Michal A
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Sanin,  Pena David Estaban
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Apostolova,  Petya
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Nerz,  Gabi
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Lampaki,  Dimitrios
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Mittler,  Gerhard
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Pearce,  Edward Jonathen
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Pearce,  Erika Laine
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Stanczak, M. A., Sanin, P. D. E., Apostolova, P., Nerz, G., Lampaki, D., Hofmann, M., et al. (2021). IL-33 expression in response to SARS-CoV-2 correlates with seropositivity in COVID-19 convalescent individuals. Nature Communications, 12, 2133. doi:10.1038/s41467-021-22449-w.


Cite as: http://hdl.handle.net/21.11116/0000-0008-4D91-E
Abstract
Our understanding of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is still developing. We perform an observational study to investigate seroprevalence and immune responses in subjects professionally exposed to SARS-CoV-2 and their family members (155 individuals; ages 5-79 years). Seropositivity for SARS-CoV-2 Spike glycoprotein aligns with PCR results that confirm the previous infection. Anti-Spike IgG/IgM titers remain high 60 days post-infection and do not strongly associate with symptoms, except for fever. We analyze PBMCs from a subset of seropositive and seronegative adults. TLR7 agonist-activation reveals an increased population of IL-6+TNF-IL-1β+ monocytes, while SARS-CoV-2 peptide stimulation elicits IL-33, IL-6, IFNa2, and IL-23 expression in seropositive individuals. IL-33 correlates with CD4+ T cell activation in PBMCs from convalescent subjects and is likely due to T cell-mediated effects on IL-33-producing cells. IL-33 is associated with pulmonary infection and chronic diseases like asthma and COPD, but its role in COVID-19 is unknown. Analysis of published scRNAseq data of bronchoalveolar lavage fluid (BALF) from patients with mild to severe COVID-19 reveals a population of IL-33-producing cells that increases with the disease. Together these findings show that IL-33 production is linked to SARS-CoV-2 infection and warrant further investigation of IL-33 in COVID-19 pathogenesis and immunity.