http://purl.uniprot.org/citations/25415279 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/25415279 | http://www.w3.org/2000/01/rdf-schema#comment | "Interleukin 34 (IL-34) is a newly recognized cytokine that functions similarly to macrophage colony-stimulating factor. This study investigated the mechanism by which IL-34 is produced in response to exogenous pathogen infections in humans. The results showed that the IL-34 levels were higher in the serum and peripheral blood mononuclear cells (PBMCs) from 155 influenza A virus (IAV)-infected patients than in those from 145 healthy individuals. The expression level of IL-34 in IAV-infected PBMCs was blocked by IL-22-specific siRNA. This result indicated that IL-34 was induced by IL-22 in the inflammatory cascade. The mRNA and protein expression levels of IL-22 activated by IAV infection were significantly inhibited by IL-34 overexpression but induced by IL-34-specific siRNA. Thus, a feedback system most likely exists between IL-34 and IL-22. The IL-22 expression in T helper type 17 (Th17) cells of PBMCs was higher than IL-34 expression in Th17 cells of PBMCs, and there was IL-34 expression in IL-22+ Th17 cells. This result showed that the production of IL-22 and IL-34 is both from the same and different subset of cells, which indicated that the regulatory mechanism of IL-22/IL-34 is through the autocrine or paracrine systems. In conclusion, IL-34 is induced by IL-22 in the inflammatory cascade in response to IAV infection. Therefore, IL-34 is a promising target for the screening of anti-inflammatory medicines."xsd:string |
http://purl.uniprot.org/citations/25415279 | http://purl.org/dc/terms/identifier | "doi:10.1097/maj.0000000000000373"xsd:string |
http://purl.uniprot.org/citations/25415279 | http://purl.uniprot.org/core/author | "Liu Z."xsd:string |
http://purl.uniprot.org/citations/25415279 | http://purl.uniprot.org/core/author | "Li Y."xsd:string |
http://purl.uniprot.org/citations/25415279 | http://purl.uniprot.org/core/author | "Li W."xsd:string |
http://purl.uniprot.org/citations/25415279 | http://purl.uniprot.org/core/author | "Yu G."xsd:string |
http://purl.uniprot.org/citations/25415279 | http://purl.uniprot.org/core/author | "Zhu S."xsd:string |
http://purl.uniprot.org/citations/25415279 | http://purl.uniprot.org/core/author | "Xia L."xsd:string |
http://purl.uniprot.org/citations/25415279 | http://purl.uniprot.org/core/author | "Bing Y."xsd:string |
http://purl.uniprot.org/citations/25415279 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
http://purl.uniprot.org/citations/25415279 | http://purl.uniprot.org/core/name | "Am J Med Sci"xsd:string |
http://purl.uniprot.org/citations/25415279 | http://purl.uniprot.org/core/pages | "145-150"xsd:string |
http://purl.uniprot.org/citations/25415279 | http://purl.uniprot.org/core/title | "Activation of the interleukin-34 inflammatory pathway in response to influenza A virus infection."xsd:string |
http://purl.uniprot.org/citations/25415279 | http://purl.uniprot.org/core/volume | "349"xsd:string |
http://purl.uniprot.org/citations/25415279 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/25415279 |
http://purl.uniprot.org/citations/25415279 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/25415279 |
http://purl.uniprot.org/uniprot/#_Q6ZMJ4-mappedCitation-25415279 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/25415279 |
http://purl.uniprot.org/uniprot/Q6ZMJ4 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/25415279 |