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http://purl.uniprot.org/citations/23659670http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23659670http://www.w3.org/2000/01/rdf-schema#comment"Recent studies suggest that dysregulated innate immunity plays an important role in the pathogenesis of immunoglobulin A nephropathy (IgAN). The interleukin-20 subfamily and its receptor, interleukin-22 receptor alpha-1 (IL-22R1), were recently identified as immunomodulators in human diseases, acting as mediators of mucosal host defense. However, the potential role of IL-22R1 in the pathogenesis of IgAN has not been explored. In the current study, 194 patients with IgAN and 287 normal controls were genotyped for coding polymorphisms of the IL-22R1 gene and the association between the polymorphisms and IgAN was investigated. Local expression of IL-22R1 was examined in patients with IgAN and healthy controls using immunohistochemistry. Our case-control analysis showed that genotypes of rs3795299 were associated with childhood IgAN. Individuals with the CC genotype of rs3795299 had about 3-fold reduced risk of IgAN compared with those with the GG genotype in the codominant model (P=0.0028) and those with the genotypes containing the G allele (GG or GC) in the recessive model (P=0.002). After Bonferroni correction, the association between the rs3795299 CC genotype and reduced risk of developing IgAN remained significant. Furthermore, the renal expression of IL-22R1 was significantly higher in healthy controls compared with subjects with IgAN. Our data suggest that the CC genotype of rs3795299 polymorphism in the IL-22R1 gene is associated with the reduced risk of IgAN, and this genetic association was supported by the higher renal expression of IL-22R1 in healthy controls compared with patients with IgAN."xsd:string
http://purl.uniprot.org/citations/23659670http://purl.org/dc/terms/identifier"doi:10.1089/jir.2012.0097"xsd:string
http://purl.uniprot.org/citations/23659670http://purl.uniprot.org/core/author"Park Y.K."xsd:string
http://purl.uniprot.org/citations/23659670http://purl.uniprot.org/core/author"Moon A."xsd:string
http://purl.uniprot.org/citations/23659670http://purl.uniprot.org/core/author"Cho S.H."xsd:string
http://purl.uniprot.org/citations/23659670http://purl.uniprot.org/core/author"Chung J.H."xsd:string
http://purl.uniprot.org/citations/23659670http://purl.uniprot.org/core/author"Suh J.S."xsd:string
http://purl.uniprot.org/citations/23659670http://purl.uniprot.org/core/author"Cho B.S."xsd:string
http://purl.uniprot.org/citations/23659670http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23659670http://purl.uniprot.org/core/name"J Interferon Cytokine Res"xsd:string
http://purl.uniprot.org/citations/23659670http://purl.uniprot.org/core/pages"571-577"xsd:string
http://purl.uniprot.org/citations/23659670http://purl.uniprot.org/core/title"A polymorphism of interleukin-22 receptor alpha-1 is associated with the development of childhood IgA nephropathy."xsd:string
http://purl.uniprot.org/citations/23659670http://purl.uniprot.org/core/volume"33"xsd:string
http://purl.uniprot.org/citations/23659670http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23659670
http://purl.uniprot.org/citations/23659670http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23659670
http://purl.uniprot.org/uniprot/#_B4E2V9-mappedCitation-23659670http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23659670
http://purl.uniprot.org/uniprot/#_Q8N6P7-mappedCitation-23659670http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23659670
http://purl.uniprot.org/uniprot/B4E2V9http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/23659670
http://purl.uniprot.org/uniprot/Q8N6P7http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/23659670