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This infection phenotype is suggestive of defects in neutrophils, but data on neutrophil functions in HIES are inconsistent. This study was undertaken to functionally characterize neutrophils in STAT3\u2010deficient HIES patients and to analyze whether the patients` eosinophilia affects the neutrophil phenotype in <jats:italic>S. aureus<\/jats:italic> infection. Neutrophil functions and cell death kinetics were studied in eight STAT3\u2010deficient patients. Moreover, the response of STAT3\u2010deficient neutrophils to <jats:italic>S. aureus<\/jats:italic> and the impact of autologous eosinophils on pathogen\u2010induced cell death were analyzed. No specific aberrations in neutrophil functions were detected within this cohort. However, the half\u2010life of STAT3\u2010deficient neutrophils ex vivo was reduced, which was partially attributable to the presence of eosinophils. Increased <jats:italic>S. aureus\u2010<\/jats:italic>induced cell lysis, dependent on the staphylococcal virulence controlling accessory gene regulator (<jats:italic>agr<\/jats:italic>)\u2010locus, was observed in STAT3\u2010deficient neutrophils and upon addition of eosinophils. Accelerated neutrophil cell death kinetics may underlie the reported variability in neutrophil function testing in HIES. Increased <jats:italic>S. aureus<\/jats:italic>\u2010induced lysis of STAT3\u2010deficient neutrophils might affect pathogen control and contribute to tissue destruction during staphylococcal infections in HIES.<\/jats:p>","DOI":"10.1002\/eji.201847650","type":"journal-article","created":{"date-parts":[[2018,10,13]],"date-time":"2018-10-13T14:59:52Z","timestamp":1539442792000},"page":"1975-1988","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Eosinophilia and reduced STAT3 signaling affect neutrophil cell death in autosomal\u2010dominant Hyper\u2010IgE syndrome"],"prefix":"10.1002","volume":"48","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8441-1784","authenticated-orcid":false,"given":"Susan","family":"Farmand","sequence":"first","affiliation":[{"name":"Department of Clinical Microbiology Karolinska University Hospital  Solna Sweden"},{"name":"Department of Microbiology Tumor and Cell Biology Karolinska 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Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Bergman","sequence":"additional","affiliation":[{"name":"Department of Clinical Microbiology Karolinska University Hospital  Solna Sweden"},{"name":"Department of Laboratory Medicine Clinical Microbiology Karolinska Institutet  Stockholm Sweden"},{"name":"Immunodeficiency Unit, Infectious Disease Clinic Karolinska University Hospital  Huddinge Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mikael","family":"Sundin","sequence":"additional","affiliation":[{"name":"Section of Hematology Immunology and HSCT Astrid Lindgren Children's Hospital Karolinska University Hospital  Stockholm Sweden"},{"name":"Department of Clinical Science Intervention and Technology Karolinska Institutet  Stockholm Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henrike","family":"Ritterbusch","sequence":"additional","affiliation":[{"name":"Center for Chronic Immunodeficiency 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