<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Woelk J</submitter><funding>Austrian Science Fund FWF</funding><funding>Tirolean Science Fund and Matching Funds Tirol:</funding><funding>Christian Doppler Society Austria (C. Doppler Laboratory for Iron and Anemia Research)</funding><pagination>e04280</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12499465</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(37)</volume><pubmed_abstract>Nuclear receptors regulate key functions of mononuclear phagocytes and are critical components of the innate immune system, acting as regulators of organ health and disease. In healthy mice, the loss of the nuclear orphan receptor NR2F6 alters tissue-resident macrophage populations in the liver, lung, and spleen. In response to Salmonella Typhimurium infection, Nr2f6-deficient mice exhibit improved clinical outcomes, characterized by reduced weight loss, bacterial loads in the spleen and liver, and decreased plasma pro-inflammatory cytokines. Despite unchanged basal iron metabolism in the spleen and liver, iron regulatory proteins and the interleukin (IL)-6-hepcidin axis are altered in Nr2f6-deficient mice during Salmonella infection, reducing hypoferremia. Transcriptomic analysis of splen</pubmed_abstract><journal>Advanced science (Weinheim, Baden-Wurttemberg, Germany)</journal><pubmed_title>Loss of NR2F6 Protects from Salmonella Typhimurium Infection.</pubmed_title><pmcid>PMC12499465</pmcid><funding_grant_id>DOI10.55776/DOC82</funding_grant_id><funding_grant_id>DOI10.55776/P28694</funding_grant_id><funding_grant_id>F.30904/7-2021</funding_grant_id><funding_grant_id>DOI10.55776/PAT6014624</funding_grant_id><pubmed_authors>Hermann M</pubmed_authors><pubmed_authors>Kleiter A</pubmed_authors><pubmed_authors>Brigo N</pubmed_authors><pubmed_authors>Pfeifhofer-Obermair C</pubmed_authors><pubmed_authors>Weiss G</pubmed_authors><pubmed_authors>Bamberger M</pubmed_authors><pubmed_authors>Hermann-Kleiter N</pubmed_authors><pubmed_authors>Benz J</pubmed_authors><pubmed_authors>Woelk J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Loss of NR2F6 Protects from Salmonella Typhimurium Infection.</name><description>Nuclear receptors regulate key functions of mononuclear phagocytes and are critical components of the innate immune system, acting as regulators of organ health and disease. In healthy mice, the loss of the nuclear orphan receptor NR2F6 alters tissue-resident macrophage populations in the liver, lung, and spleen. In response to Salmonella Typhimurium infection, Nr2f6-deficient mice exhibit improved clinical outcomes, characterized by reduced weight loss, bacterial loads in the spleen and liver, and decreased plasma pro-inflammatory cytokines. Despite unchanged basal iron metabolism in the spleen and liver, iron regulatory proteins and the interleukin (IL)-6-hepcidin axis are altered in Nr2f6-deficient mice during Salmonella infection, reducing hypoferremia. Transcriptomic analysis of splen</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Oct</publication><modification>2026-06-04T05:45:37.347Z</modification><creation>2026-05-05T03:13:17.705Z</creation></dates><accession>S-EPMC12499465</accession><cross_references><pubmed>40605423</pubmed><doi>10.1002/advs.202404280</doi></cross_references></HashMap>