title: Polymorphisms of interleukin-4--related genes in Japanese children with minimal change nephrotic syndrome.
abstract: BACKGROUND
  Minimal change nephrotic syndrome (MCNS) in children frequently is associated with allergy and immunoglobulin E production. T Helper subtype 2 cytokines, such as interleukin-4 (IL-4), may have an important role in the development of atopy. We investigated the associations of gene polymorphisms of IL-4, its receptor (IL-4R), and the signal transducer and activator 6 (STAT6) gene with MCNS.
  
  
  METHODS
  We analyzed these polymorphisms in Japanese children with MCNS (n = 58) and healthy controls with neither allergic nor renal disease (n = 63). The polymerase chain reaction (PCR) and restriction fragment length polymorphism method was used for the IL-4 promoter gene polymorphism (-590C/T), and PCR single-strand conformation polymorphism analysis was used for the IL-4Ralpha chain gene (1902A/G) and STAT6 3' untranslated region (2964G/A) polymorphisms.
  
  
  RESULTS
  There was a significant difference between the MCNS group and controls in genotypic distribution of IL-4 promoter gene polymorphism. Frequency of the T allele was significantly lower in the MCNS group than controls. There was no difference between the MCNS group and controls in the IL-4R gene polymorphism. In the STAT6 gene, no significant differences in genotypic and allelic distribution were observed between the 2 groups. However, there were significant differences between patients who did not need cytotoxic agents or who experienced 3 or fewer relapses and controls.
  
  
  CONCLUSIONS
  These results suggest that genetic variations in the IL-4 and STAT6 genes may be associated with predisposition to MCNS, partially the clinical course of MCNS.
authors.affiliation: Department of Pediatrics, Gunma University School of Medicine, Maebashi, Gunma, Japan.
authors.forename: Yasuko
authors.initials: Y
authors.lastname: Kobayashi
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Arakawa
authors.forename: Michiko
authors.initials: M
authors.lastname: Suzuki
authors.forename: Takumi
authors.initials: T
authors.lastname: Takizawa
authors.forename: Kenichi
authors.initials: K
authors.lastname: Tokuyama
authors.forename: Akihiro
authors.initials: A
authors.lastname: Morikawa
mesh_terms: D000293:Adolescent; D002648:Child; D002675:Child, Preschool; D018450:Disease Progression; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D006967:Hypersensitivity / Q000235:genetics; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007223:Infant; D015847:Interleukin-4 / Q000235:genetics*; D007564:Japan / Q000453:epidemiology; D008297:Male; D009402:Nephrosis, Lipoid / Q000188:drug therapy / Q000208:ethnology / Q000235:genetics*; D009404:Nephrotic Syndrome / Q000188:drug therapy / Q000208:ethnology / Q000235:genetics*; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D018807:Polymorphism, Single-Stranded Conformational; D011401:Promoter Regions, Genetic; D019948:Receptors, Interleukin-4 / Q000235:genetics*; D012008:Recurrence; D050800:STAT6 Transcription Factor; D015534:Trans-Activators / Q000235:genetics*
chemical_list: D007166:Immunosuppressive Agents; D019948:Receptors, Interleukin-4; D050800:STAT6 Transcription Factor; C494101:STAT6 protein, human; D015534:Trans-Activators; D015847:Interleukin-4