<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>52(12)</volume><submitter>Meltendorf S</submitter><pubmed_abstract>After recovery, mild and severe COVID-19 diseases are associated with long-term effects on the host immune system, such as prolonged T-cell activation or accumulation of autoantibodies. In this study, we show that mild SARS-CoV-2 infections, but not SARS-CoV-2 spike mRNA vaccinations, cause durable atopic risk factors such as a systemic Th2- and Th17-type environment as well as activation of B cells responsive of IgE against aeroallergens from house dust mite and mold. At an average of 100 days post mild SARS-CoV-2 infections, anti-mold responses were associated with low IL-13 levels and increased pro-inflammatory IL-6 titers. Acutely severely ill COVID-19 patients instead showed no evidence of atopic reactions. Considering convalescents of mild COVID-19 courses and mRNA-vaccinated individuals together, IL-13 was the predominant significantly upregulated factor, likely shaping SARS-CoV-2 immunity. Application of multiple regression analysis revealed that the IL-13 levels of both groups were determined by the Th17-type cytokines IL-17A and IL-22. Taken together, these results implicate a critical role for IL-13 in the aftermath of SARS-CoV-2 mild infections and mRNA vaccinations, conferring protection against airway directed, atopic side reactions that occur in mildly experienced COVID-19.</pubmed_abstract><journal>European journal of immunology</journal><pagination>1972-1979</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9874813</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>IL-13 determines specific IgE responses and SARS-CoV-2 immunity after mild COVID-19 and novel mRNA vaccination.</pubmed_title><pmcid>PMC9874813</pmcid><pubmed_authors>Schraven B</pubmed_authors><pubmed_authors>Hachenberg T</pubmed_authors><pubmed_authors>Kaasch AJ</pubmed_authors><pubmed_authors>Brunner-Weinzierl MC</pubmed_authors><pubmed_authors>Farber J</pubmed_authors><pubmed_authors>Reinhold A</pubmed_authors><pubmed_authors>Reinhold D</pubmed_authors><pubmed_authors>Lingel H</pubmed_authors><pubmed_authors>Pratsch F</pubmed_authors><pubmed_authors>Thurm C</pubmed_authors><pubmed_authors>Meltendorf S</pubmed_authors><pubmed_authors>Heuft HG</pubmed_authors><pubmed_authors>Vogel K</pubmed_authors><pubmed_authors>Weinzierl S</pubmed_authors></additional><is_claimable>false</is_claimable><name>IL-13 determines specific IgE responses and SARS-CoV-2 immunity after mild COVID-19 and novel mRNA vaccination.</name><description>After recovery, mild and severe COVID-19 diseases are associated with long-term effects on the host immune system, such as prolonged T-cell activation or accumulation of autoantibodies. In this study, we show that mild SARS-CoV-2 infections, but not SARS-CoV-2 spike mRNA vaccinations, cause durable atopic risk factors such as a systemic Th2- and Th17-type environment as well as activation of B cells responsive of IgE against aeroallergens from house dust mite and mold. At an average of 100 days post mild SARS-CoV-2 infections, anti-mold responses were associated with low IL-13 levels and increased pro-inflammatory IL-6 titers. Acutely severely ill COVID-19 patients instead showed no evidence of atopic reactions. Considering convalescents of mild COVID-19 courses and mRNA-vaccinated individuals together, IL-13 was the predominant significantly upregulated factor, likely shaping SARS-CoV-2 immunity. Application of multiple regression analysis revealed that the IL-13 levels of both groups were determined by the Th17-type cytokines IL-17A and IL-22. Taken together, these results implicate a critical role for IL-13 in the aftermath of SARS-CoV-2 mild infections and mRNA vaccinations, conferring protection against airway directed, atopic side reactions that occur in mildly experienced COVID-19.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2024-11-08T19:41:52.383Z</modification><creation>2024-11-08T19:41:52.383Z</creation></dates><accession>S-EPMC9874813</accession><cross_references><pubmed>36271745</pubmed><doi>10.1002/eji.202249951</doi></cross_references></HashMap>