biostudies-literatureHenry TNIAID NIH HHS3755-67https://www.ebi.ac.uk/biostudies/studies/S-EPMC2879132biostudies-literatureUnknown184(7)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 oJournal of immunology (Baltimore, Md. : 1950)Type I IFN signaling constrains IL-17A/F secretion by gammadelta T cells during bacterial infections.PMC2879132P01 AI063302P01 AI 56320U54 AI065359-066080AI 063302P01 AI056320U54 AI065359P01 AI063302-068612P01 AI056320-06A2AI065359T32 AI007328Perret MHenry TKirimanjeswara GSHo LRuby TMetzger DWMonack DMJones JWIwakura YSauer JDPeng KfalseType I IFN signaling constrains IL-17A/F secretion by gammadelta T cells during bacterial infections.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 o2010-01-01T00:00:00Z2010 Apr2025-04-22T06:47:26.877Z2019-03-26T23:42:52ZS-EPMC28791322017674410.4049/jimmunol.0902065