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Evidence suggests that dysregulated immune responses, including autoimmunity, are key pathogenic factors.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To assess whether IgA autoantibodies target lung-specific proteins and contribute to disease severity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We collected 147 blood, 9 lung tissue, and 36 BAL fluid samples from three tertiary hospitals in Switzerland and one in Germany. Severe COVID-19 was defined by the need to administer oxygen. We investigated the presence of IgA autoantibodies and their effects on pulmonary surfactant in COVID-19 using the following methods: immunofluorescence on tissue samples, immunoprecipitations followed by mass spectrometry on BAL fluid samples, enzyme-linked immunosorbent assays on blood samples, and surface tension measurements with medical surfactant.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>IgA autoantibodies targeting pulmonary surfactant proteins B and C were elevated in patients with severe COVID-19 but not in patients with influenza or bacterial pneumonia. Notably, pulmonary surfactant failed to reduce surface tension after incubation with either plasma or purified IgA from patients with severe COVID-19.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our data suggest that patients with severe COVID-19 harbor IgA autoantibodies against pulmonary surfactant proteins B and C and that these autoantibodies block the function of lung surfactant, potentially contributing to alveolar collapse and poor oxygenation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.202201-0011oc","type":"journal-article","created":{"date-parts":[[2022,8,4]],"date-time":"2022-08-04T15:55:37Z","timestamp":1659628537000},"page":"38-49","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":33,"title":["Pulmonary Surfactant Proteins Are Inhibited by Immunoglobulin A Autoantibodies in Severe COVID-19"],"prefix":"10.1093","volume":"207","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3922-3327","authenticated-orcid":false,"given":"Tobias","family":"Sinnberg","sequence":"first","affiliation":[{"name":"Department of Dermatology"},{"name":"Cluster of Excellence iFIT (EXC 2180) Image Guided and Functionally Instructed Tumor Therapies"},{"name":"Department of Dermatology, Venereology and Allergology, Charit\u00e9-Universit\u00e4tsmedizin Berlin, Charit\u00e9platz 1, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christa","family":"Lichtensteiger","sequence":"additional","affiliation":[{"name":"Institute of Immunobiology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5185-7520","authenticated-orcid":false,"given":"Omar Hasan","family":"Ali","sequence":"additional","affiliation":[{"name":"Institute of Immunobiology"},{"name":"Department of Medical Genetics, Life Sciences Institute, University of 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