| http://purl.uniprot.org/citations/20176744 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20176744 | http://www.w3.org/2000/01/rdf-schema#comment | "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 of IL-17A(+) gammadelta T cells during infection. Furthermore, IL-17A-deficient mice contained fewer neutrophils compared with wild-type mice during infection, indicating that IL-17A contributes to neutrophil expansion during F. novicida infection. Accordingly, an increase in IL-17A in IFNAR1(-/-) mice correlated with an increase in splenic neutrophil numbers. Similar results were obtained in a mouse model of pneumonic tularemia using the highly virulent F. tularensis subspecies tularensis SchuS4 strain and in a mouse model of systemic Listeria monocytogenes infection. Our results indicate that the type I IFN-mediated negative regulation of IL-17A(+) gammadelta T cell expansion is conserved during bacterial infections. We propose that this newly described activity of type I IFN signaling might participate in the resistance of the IFNAR1(-/-) mice to infection with F. novicida and other intracellular bacteria."xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.0902065"xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/author | "Monack D.M."xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/author | "Ho L."xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/author | "Jones J.W."xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/author | "Peng K."xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/author | "Iwakura Y."xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/author | "Henry T."xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/author | "Perret M."xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/author | "Sauer J.D."xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/author | "Kirimanjeswara G.S."xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/author | "Metzger D.W."xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/author | "Ruby T."xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/pages | "3755-3767"xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/title | "Type I IFN signaling constrains IL-17A/F secretion by gammadelta T cells during bacterial infections."xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://purl.uniprot.org/core/volume | "184"xsd:string |
| http://purl.uniprot.org/citations/20176744 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/20176744 |
| http://purl.uniprot.org/citations/20176744 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/20176744 |
| http://purl.uniprot.org/uniprot/#_A0A087WQB4-mappedCitation-20176744 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/20176744 |
| http://purl.uniprot.org/uniprot/#_A0A338P6T9-mappedCitation-20176744 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/20176744 |
| http://purl.uniprot.org/uniprot/#_A0A338P6X7-mappedCitation-20176744 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/20176744 |
| http://purl.uniprot.org/uniprot/#_A0A384DVB8-mappedCitation-20176744 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/20176744 |