| http://purl.uniprot.org/citations/22651933 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22651933 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22651933 | http://www.w3.org/2000/01/rdf-schema#comment | "The resolution of acute inflammation is hallmarked by the apoptotic death of inflammatory polymorphonuclear (PMN) cells, followed by their clearance by macrophages. In turn, resolution-phase macrophages exert reduced proinflammatory cytokine production, termed immune silencing. In this study, we found that the atypical chemokine receptor D6 plays an important and chemokine scavenging-independent role in promoting macrophage-mediated resolution. D6(-/-) mice displayed increased numbers of macrophages (2.2-fold increase), but not neutrophils, in their peritonea during the resolution of murine zymosan A-initiated peritonitis, in comparison to D6(+/+) animals. Moreover, D6-deficient macrophages engulfed higher numbers of apoptotic PMN cells in vivo (1.6-fold increase), and secreted higher amounts of TNF-α, CCL3, and CCL5 ex vivo than their wild-type (WT) counterparts. In addition, D6 was found to be expressed on apoptotic neutrophils from healthy humans and rodents. Moreover, the immune silencing of LPS-stimulated macrophages following their incubation with senescent PMN cells ex vivo (in terms of TNF-α, IL-1β, and CCL5 secretion) was diminished (50-65% decrease) when D6(-/-) PMN cells were applied. Accordingly, the adhesive responses induced by macrophage interactions with senescent PMN cells were reduced with D6-deficient PMN cells. Thus, our results indicate a novel mode of action for D6 during the resolution of inflammation that is instrumental to the shaping of resolving macrophage phenotypes and the completion of resolution."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.org/dc/terms/identifier | "doi:10.1096/fj.11-194894"xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.org/dc/terms/identifier | "doi:10.1096/fj.11-194894"xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/author | "Shapiro H."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/author | "Shapiro H."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/author | "Ariel A."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/author | "Ariel A."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/author | "Aswad M."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/author | "Aswad M."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/author | "Pashover-Schallinger E."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/author | "Pashover-Schallinger E."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/author | "Schif-Zuck S."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/author | "Schif-Zuck S."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/author | "Singer P."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/author | "Singer P."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/name | "FASEB J."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/name | "FASEB J."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/pages | "3891-3900"xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/pages | "3891-3900"xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/title | "The atypical chemokine receptor D6 controls macrophage efferocytosis and cytokine secretion during the resolution of inflammation."xsd:string |
| http://purl.uniprot.org/citations/22651933 | http://purl.uniprot.org/core/title | "The atypical chemokine receptor D6 controls macrophage efferocytosis and cytokine secretion during the resolution of inflammation."xsd:string |