| http://purl.uniprot.org/citations/21998459 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21998459 | http://www.w3.org/2000/01/rdf-schema#comment | "Allergic inflammation in the airway is generally considered a Th2-type immune response. However, Th17-type immune responses also play important roles in this process, especially in the pathogenesis of severe asthma. IL-22 is a Th17-type cytokine and thus might play roles in the development of allergic airway inflammation. There is increasing evidence that IL-22 can act as a proinflammatory or anti-inflammatory cytokine depending on the inflammatory context. However, its role in Ag-induced immune responses is not well understood. This study examined whether IL-22 could suppress allergic airway inflammation and its mechanism of action. BALB/c mice were sensitized and challenged with OVA-Ag to induce airway inflammation. An IL-22-producing plasmid vector was delivered before the systemic sensitization or immediately before the airway challenge. Delivery of the IL-22 gene before sensitization, but not immediately before challenge, suppressed eosinophilic airway inflammation. IL-22 gene delivery suppressed Ag-induced proliferation and overall cytokine production in CD4(+) T cells, indicating that it could suppress Ag-induced T cell priming. Antagonism of IL-22 by IL-22-binding protein abolished IL-22-induced immune suppression, suggesting that IL-22 protein itself played an essential role. IL-22 gene delivery neither increased regulatory T cells nor suppressed dendritic cell functions. The suppression by IL-22 was abolished by deletion of the IL-10 gene or neutralization of the IL-10 protein. Finally, IL-22 gene delivery increased IL-10 production in draining lymph nodes. These findings suggested that IL-22 could have an immunosuppressive effect during the early stage of an immune response. Furthermore, IL-10 plays an important role in the immune suppression by IL-22."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1001560"xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/author | "Chang H."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/author | "Miyazaki J."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/author | "Matsumoto T."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/author | "Yamamoto K."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/author | "Tanaka R."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/author | "Imamura M."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/author | "Harada H."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/author | "Hanawa H."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/author | "Nakagome K."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/author | "Kano M.R."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/author | "Kawahata K."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/author | "Sasaki O."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/author | "Dohi M."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/author | "Okunishi K."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/pages | "5077-5089"xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/title | "High expression of IL-22 suppresses antigen-induced immune responses and eosinophilic airway inflammation via an IL-10-associated mechanism."xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://purl.uniprot.org/core/volume | "187"xsd:string |
| http://purl.uniprot.org/citations/21998459 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/21998459 |
| http://purl.uniprot.org/citations/21998459 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/21998459 |
| http://purl.uniprot.org/uniprot/#_A0A7R8C389-mappedCitation-21998459 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21998459 |