{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Henry T"],"funding":["NIAID NIH HHS"],"pagination":["3755-67"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2879132"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["184(7)"],"pubmed_abstract":["Recognition of intracellular bacteria by macrophages leads to secretion of type I IFNs. However, the role of type I IFN during bacterial infection is still poorly understood. Francisella tularensis, the causative agent of tularemia, is a pathogenic bacterium that replicates in the cytosol of macrophages leading to secretion of type I IFN. In this study, we investigated the role of type I IFNs in a mouse model of tularemia. Mice deficient for type I IFN receptor (IFNAR1(-/-)) are more resistant to intradermal infection with F. tularensis subspecies novicida (F. novicida). Increased resistance to infection was associated with a specific increase in IL-17A/F and a corresponding expansion of an IL-17A(+) gammadelta T cell population, indicating that type I IFNs negatively regulate the number o"],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["Type I IFN signaling constrains IL-17A/F secretion by gammadelta T cells during bacterial infections."],"pmcid":["PMC2879132"],"funding_grant_id":["P01 AI063302","P01 AI 56320","U54 AI065359-066080","AI 063302","P01 AI056320","U54 AI065359","P01 AI063302-068612","P01 AI056320-06A2","AI065359","T32 AI007328"],"pubmed_authors":["Perret M","Henry T","Kirimanjeswara GS","Ho L","Ruby T","Metzger DW","Monack DM","Jones JW","Iwakura Y","Sauer JD","Peng K"],"additional_accession":[]},"is_claimable":false,"name":"Type I IFN signaling constrains IL-17A/F secretion by gammadelta T cells during bacterial infections.","description":"Recognition of intracellular bacteria by macrophages leads to secretion of type I IFNs. However, the role of type I IFN during bacterial infection is still poorly understood. Francisella tularensis, the causative agent of tularemia, is a pathogenic bacterium that replicates in the cytosol of macrophages leading to secretion of type I IFN. In this study, we investigated the role of type I IFNs in a mouse model of tularemia. Mice deficient for type I IFN receptor (IFNAR1(-/-)) are more resistant to intradermal infection with F. tularensis subspecies novicida (F. novicida). Increased resistance to infection was associated with a specific increase in IL-17A/F and a corresponding expansion of an IL-17A(+) gammadelta T cell population, indicating that type I IFNs negatively regulate the number o","dates":{"release":"2010-01-01T00:00:00Z","publication":"2010 Apr","modification":"2025-04-22T06:47:26.877Z","creation":"2019-03-26T23:42:52Z"},"accession":"S-EPMC2879132","cross_references":{"pubmed":["20176744"],"doi":["10.4049/jimmunol.0902065"]}}