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In healthy mice, the loss of the nuclear orphan receptor NR2F6 alters tissue\u2010resident macrophage populations in the liver, lung, and spleen. In response to\n                    <jats:italic>Salmonella<\/jats:italic>\n                    Typhimurium infection,\n                    <jats:italic>Nr2f6<\/jats:italic>\n                    \u2010deficient mice exhibit improved clinical outcomes, characterized by reduced weight loss, bacterial loads in the spleen and liver, and decreased plasma pro\u2010inflammatory cytokines. Despite unchanged basal iron metabolism in the spleen and liver, iron regulatory proteins and the interleukin (IL)\u20106\u2010hepcidin axis are altered in\n                    <jats:italic>Nr2f6\u2010<\/jats:italic>\n                    deficient mice during\n                    <jats:italic>Salmonella<\/jats:italic>\n                    infection, reducing hypoferremia. Transcriptomic analysis of splenic red pulp macrophages reveals significant alterations of phagocytosis\u2010related genes, including upregulation of signal\u2010regulatory protein alpha (Sirpa). In vitro, phagocytosis of red blood cells, regulated by the inhibitory CD47\u2010Sirp\u03b1 axis, and\n                    <jats:italic>Salmonella<\/jats:italic>\n                    Typhimurium phagocytosis are significantly impaired in\n                    <jats:italic>Nr2f6<\/jats:italic>\n                    \u2010deficient splenic macrophages. Blocking Sirp\u03b1 in vitro restores the phagocytic activity of\n                    <jats:italic>Nr2f6<\/jats:italic>\n                    \u2010deficient macrophages to wild\u2010type levels. In vivo\n                    <jats:italic>, Salmonella<\/jats:italic>\n                    Typhimurium loads are partially increased post\u2010infection in anti\u2010Sirp\u03b1 treated\n                    <jats:italic>Nr2f6<\/jats:italic>\n                    \u2010deficient mice. These findings uncover a previously unrecognized role of NR2F6 in host\u2010pathogen interactions, positioning it as a potential therapeutic target for infectious diseases.\n                  <\/jats:p>","DOI":"10.1002\/advs.202404280","type":"journal-article","created":{"date-parts":[[2025,7,3]],"date-time":"2025-07-03T02:29:03Z","timestamp":1751509743000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Loss of NR2F6 Protects from\n                    <i>Salmonella<\/i>\n                    Typhimurium Infection"],"prefix":"10.1002","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3535-5576","authenticated-orcid":false,"given":"Johannes","family":"Woelk","sequence":"first","affiliation":[{"name":"Institute of Cell Genetics Department for Genetics Medical University of Innsbruck  Innsbruck 6020 Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9942-6540","authenticated-orcid":false,"given":"Christa","family":"Pfeifhofer\u2010Obermair","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II (Infectious Diseases, Immunology, Rheumatology, Pneumology) Medical University of Innsbruck  Innsbruck 6020 Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia","family":"Benz","sequence":"additional","affiliation":[{"name":"Institute of Cell Genetics Department for Genetics Medical University of Innsbruck  Innsbruck 6020 Austria"},{"name":"Institute of Microbiology \u2013 Clinical Microbiology, Immunology and Hygiene University Clinic Erlangen Friedrich\u2010Alexander\u2010University Erlangen\u2010Nuremberg  91054 Erlangen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natascha","family":"Brigo","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II (Infectious Diseases, Immunology, Rheumatology, Pneumology) Medical University of Innsbruck  Innsbruck 6020 Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Milena","family":"Bamberger","sequence":"additional","affiliation":[{"name":"Institute of Cell Genetics Department for Genetics Medical University of Innsbruck  Innsbruck 6020 Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexeja","family":"Kleiter","sequence":"additional","affiliation":[{"name":"Institute of Cell Genetics Department for Genetics Medical University of Innsbruck  Innsbruck 6020 Austria"},{"name":"Laboratory for Langerhans Cell Research Department of Dermatology Venereology &amp; 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