| http://purl.uniprot.org/citations/25267883 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/25267883 | http://www.w3.org/2000/01/rdf-schema#comment | "M2 macrophages have been subdivided into subtypes such as IL-4-induced M2a and IL-10-induced M2c in vitro. Although it was reported that IL-10 stimulation leads to an increase in IL-4Rα, the effect of IL-4 and IL-10 in combination with macrophage subtype differentiation remains unclear. Thus, we sought to clarify whether IL-10 enhanced the M2 phenotype induced by IL-4. In this study, we showed that IL-10 enhanced IL-4Rα expression in M-CSF-induced bone marrow-derived macrophages (BMDMs). Global gene expression analysis of M2 macrophages induced by IL-4, IL-10 or IL-4 + IL-10 showed that IL-10 enhanced gene expression of M2a markers induced by IL-4 in M-CSF-induced BMDMs. Moreover, IL-4 and IL-10 synergistically induced CCL24 (Eotaxin-2) production. Enhanced CCL24 expression was also observed in GM-CSF-induced BMDMs and zymosan-elicited, thioglycolate-elicited and naive peritoneal macrophages. CCL24 is a CCR3 agonist and an eosinophil chemoattractant. In vitro, IL-4 + IL-10-stimulated macrophages produced a large amount of CCL24 and increased eosinophil migration, which was inhibited by anti-CCL24 antibody. We also showed that IL-4 + IL-10-stimulated (but not IL-4 or IL-10 alone) macrophages transferred into the peritoneum of C57BL/6J mice increased eosinophil infiltration into the peritoneal cavity. These results demonstrate that IL-4 + IL-10-simulated macrophages have enhanced M2a macrophage-related gene expression, CCL24 production and eosinophil infiltration-inducing activity, thereby suggesting their contribution to eosinophil-related diseases."xsd:string |
| http://purl.uniprot.org/citations/25267883 | http://purl.org/dc/terms/identifier | "doi:10.1093/intimm/dxu090"xsd:string |
| http://purl.uniprot.org/citations/25267883 | http://purl.uniprot.org/core/author | "Hayashi Y."xsd:string |
| http://purl.uniprot.org/citations/25267883 | http://purl.uniprot.org/core/author | "Yamashiro K."xsd:string |
| http://purl.uniprot.org/citations/25267883 | http://purl.uniprot.org/core/author | "Hizukuri Y."xsd:string |
| http://purl.uniprot.org/citations/25267883 | http://purl.uniprot.org/core/author | "Makita N."xsd:string |
| http://purl.uniprot.org/citations/25267883 | http://purl.uniprot.org/core/author | "Murakawa M."xsd:string |
| http://purl.uniprot.org/citations/25267883 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
| http://purl.uniprot.org/citations/25267883 | http://purl.uniprot.org/core/name | "Int Immunol"xsd:string |
| http://purl.uniprot.org/citations/25267883 | http://purl.uniprot.org/core/pages | "131-141"xsd:string |
| http://purl.uniprot.org/citations/25267883 | http://purl.uniprot.org/core/title | "IL-10 enhances the phenotype of M2 macrophages induced by IL-4 and confers the ability to increase eosinophil migration."xsd:string |
| http://purl.uniprot.org/citations/25267883 | http://purl.uniprot.org/core/volume | "27"xsd:string |
| http://purl.uniprot.org/citations/25267883 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/25267883 |
| http://purl.uniprot.org/citations/25267883 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/25267883 |
| http://purl.uniprot.org/uniprot/#_Q9JKC0-mappedCitation-25267883 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/25267883 |
| http://purl.uniprot.org/uniprot/#_Q3U0A4-mappedCitation-25267883 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/25267883 |
| http://purl.uniprot.org/uniprot/Q3U0A4 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/25267883 |
| http://purl.uniprot.org/uniprot/Q9JKC0 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/25267883 |