| http://purl.uniprot.org/citations/21715688 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21715688 | http://www.w3.org/2000/01/rdf-schema#comment | "The binding of IL-18 to IL-18Rα induces both proinflammatory and protective functions during infection, depending on the context in which it occurs. IL-18 is highly expressed in the liver of wild-type (WT) C57BL/6 mice following lethal infection with highly virulent Ixodes ovatus ehrlichia (IOE), an obligate intracellular bacterium that causes acute fatal toxic shock-like syndrome. In this study, we found that IOE infection of IL-18Rα(-/-) mice resulted in significantly less host cell apoptosis, decreased hepatic leukocyte recruitment, enhanced bacterial clearance, and prolonged survival compared with infected WT mice, suggesting a pathogenic role for IL-18/IL-18Rα in Ehrlichia-induced toxic shock. Although lack of IL-18R decreased the magnitude of IFN-γ producing type-1 immune response, enhanced resistance of IL-18Rα(-/-) mice against Ehrlichia correlated with increased proinflammatory cytokines at sites of infection, decreased systemic IL-10 production, increased frequency of protective NKT cells producing TNF-α and IFN-γ, and decreased frequency of pathogenic TNF-α-producing CD8(+) T cells. Adoptive transfer of immune WT CD8(+) T cells increased bacterial burden in IL-18Rα(-/-) mice following IOE infection. Furthermore, rIL-18 treatment of WT mice infected with mildly virulent Ehrlichia muris impaired bacterial clearance and enhanced liver injury. Finally, lack of IL-18R signal reduced dendritic cell maturation and their TNF-α production, suggesting that IL-18 might promote the adaptive pathogenic immune responses against Ehrlichia by influencing T cell priming functions of dendritic cells. Together, these results suggested that the presence or absence of IL-18R signals governs the pathogenic versus protective immunity in a model of Ehrlichia-induced immunopathology."xsd:string |
| http://purl.uniprot.org/citations/21715688 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1100092"xsd:string |
| http://purl.uniprot.org/citations/21715688 | http://purl.uniprot.org/core/author | "Fang R."xsd:string |
| http://purl.uniprot.org/citations/21715688 | http://purl.uniprot.org/core/author | "Ghose P."xsd:string |
| http://purl.uniprot.org/citations/21715688 | http://purl.uniprot.org/core/author | "Ismail N."xsd:string |
| http://purl.uniprot.org/citations/21715688 | http://purl.uniprot.org/core/author | "Forbes D."xsd:string |
| http://purl.uniprot.org/citations/21715688 | http://purl.uniprot.org/core/author | "Ballard B."xsd:string |
| http://purl.uniprot.org/citations/21715688 | http://purl.uniprot.org/core/author | "Ali A.Q."xsd:string |
| http://purl.uniprot.org/citations/21715688 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21715688 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/21715688 | http://purl.uniprot.org/core/pages | "1333-1346"xsd:string |
| http://purl.uniprot.org/citations/21715688 | http://purl.uniprot.org/core/title | "The interaction between IL-18 and IL-18 receptor limits the magnitude of protective immunity and enhances pathogenic responses following infection with intracellular bacteria."xsd:string |
| http://purl.uniprot.org/citations/21715688 | http://purl.uniprot.org/core/volume | "187"xsd:string |
| http://purl.uniprot.org/citations/21715688 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/21715688 |
| http://purl.uniprot.org/citations/21715688 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/21715688 |
| http://purl.uniprot.org/uniprot/#_A0A0A6YWA3-mappedCitation-21715688 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21715688 |
| http://purl.uniprot.org/uniprot/#_A0A1L1STF5-mappedCitation-21715688 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21715688 |
| http://purl.uniprot.org/uniprot/#_A0PJ18-mappedCitation-21715688 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21715688 |
| http://purl.uniprot.org/uniprot/#_P70380-mappedCitation-21715688 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21715688 |
| http://purl.uniprot.org/uniprot/#_K3W4N2-mappedCitation-21715688 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21715688 |
| http://purl.uniprot.org/uniprot/#_Q2PMY2-mappedCitation-21715688 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21715688 |
| http://purl.uniprot.org/uniprot/#_Q3TCJ0-mappedCitation-21715688 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21715688 |
| http://purl.uniprot.org/uniprot/#_Q61098-mappedCitation-21715688 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21715688 |
| http://purl.uniprot.org/uniprot/#_Q80SS8-mappedCitation-21715688 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21715688 |