{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T22:32:16Z","timestamp":1791844336802,"version":"4.3.4"},"reference-count":51,"publisher":"American Society for Clinical Investigation","issue":"4","license":[{"start":{"date-parts":[[2026,2,16]],"date-time":"2026-02-16T00:00:00Z","timestamp":1771200000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,2,16]]},"abstract":"<jats:p>\n                    Anaphylaxis is a life-threatening hypersensitivity reaction. Clinical observations suggest heightened susceptibility during viral infections, yet the mechanisms remain poorly defined. Here, we show that both active and passive IgG-mediated anaphylaxis were exacerbated in the setting of acute viral infection. In mice, this enhancement was driven predominantly by Fc\u03b3RIV, the homolog of human Fc\u03b3RIIIa. Fc\u03b3RIV crosslinking induced anaphylactic symptoms selectively in infected animals, with no effect in naive conditions. Among leukocytes, inflammatory monocytes emerged as the principal drivers of this lethal reaction. Viral infection triggered a strong upregulation of Fc\u03b3RIV on inflammatory monocytes, an effect absent in type I IFN receptor\u2013deficient (\n                    <jats:italic>Ifnar1<\/jats:italic>\n                    -deficient) mice. Extending these findings, we observed increased frequencies of CD16-expressing classical monocytes in patients with acute COVID-19, and murine SARS-CoV-2 infection recapitulated this phenotype. Mechanistically, Fc\u03b3RIV crosslinking during infection promoted the production of platelet-activating factor, the key mediator of mortality, in a type I IFN\u2013dependent (IFN-I\u2013dependent) manner. Together, these findings indicate that viral infection creates an immune milieu that heightens monocyte sensitivity to Fc\u03b3 receptor engagement, positioning these cells as major effectors of IgG-mediated hypersensitivity in the infected host. They further suggest that Fc receptor pathway modulation merits further investigation in contexts with heightened IFN-I responses, such as in systemic lupus erythematosus.\n                  <\/jats:p>","DOI":"10.1172\/jci192371","type":"journal-article","created":{"date-parts":[[2026,2,15]],"date-time":"2026-02-15T19:00:58Z","timestamp":1771182058000},"source":"Crossref","is-referenced-by-count":4,"title":["Type I IFN\u2013dependent Fc\u03b3RIV signaling in murine monocytes promotes lethal anaphylaxis during viral infections"],"prefix":"10.1172","volume":"136","author":[{"given":"Abdelrahman","family":"Elwy","sequence":"first","affiliation":[{"name":"Institute of Immunology, University Hospital Essen, Medical Faculty, University of Duisburg-Essen, Essen, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hossam","family":"Abdelrahman","sequence":"additional","affiliation":[{"name":"Institute of Immunology, University Hospital Essen, Medical Faculty, University of Duisburg-Essen, Essen, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia","family":"Specht","sequence":"additional","affiliation":[{"name":"Institute of Immunology, University Hospital Essen, Medical Faculty, University of Duisburg-Essen, Essen, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gina M.","family":"Ewert","sequence":"additional","affiliation":[{"name":"Institute of Immunology, University Hospital Essen, Medical Faculty, University of Duisburg-Essen, Essen, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Justa","family":"Friebus-Kardash","sequence":"additional","affiliation":[{"name":"Institute of Immunology, University Hospital Essen, Medical Faculty, University of Duisburg-Essen, Essen, Germany."},{"name":"Department of Nephrology, University Hospital Essen, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Swati","family":"Dhiman","sequence":"additional","affiliation":[{"name":"Institute of Immunology, University Hospital Essen, Medical Faculty, University of Duisburg-Essen, Essen, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia","family":"Falkenstein","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Theresa Charlotte","family":"Christ","sequence":"additional","affiliation":[{"name":"Institute of Immunology, University Hospital Essen, Medical Faculty, University of Duisburg-Essen, Essen, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elisa","family":"Wiebeck","sequence":"additional","affiliation":[{"name":"Institute of Immunology, University Hospital Essen, Medical Faculty, University of 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