title: [Up-regulation of serum- and glucocorticoid-inducible kinase 1 (SGK1) of CD4⁺ T cells is positively related to RORC and IL-17A in patients with Kawasaki disease].
abstract: OBJECTIVE
  To investigate the expression of serum- and glucocorticoid-inducible kinase 1 (SGK1) in Kawasaki disease (KD) and explore the correlations between SGK1 and Th17 cell-related cytokines [retinoic-acid-related orphan nuclear receptor C (RORC), interleukin 17A (IL-17A), IL-6] in KD.
  
  
  METHODS
  Thirty patients with KD [(2.8 ± 1.4) years old], 30 healthy volunteers [(2.6 ± 1.6) years old] and 25 patients with infectious disease (ID) [(2.2 ± 1.5) years old] were recruited. The percentage of Th17 cells in CD4⁺ T cells was analyzed using flow cytometry. The mRNA levels of RORC and SGK1 in CD4⁺ T cells were detected using real-time quantitative PCR. The serum levels of IL-17A and IL-6 were analyzed by ELISA.
  
  
  RESULTS
  Compared with healthy volunteers and patients with ID, the percentage of Th17 cells in CD4⁺ T cells significantly increased in KD [(3.57 ± 0.62)% vs (0.51 ± 0.07)% or (1.72 ± 0.36)%]. The serum levels of IL-17A and IL-6 in KD were much higher than those in healthy volunteers and patients with ID. The mRNA levels of RORC and SGK1 in KD were remarkably elevated compared with healthy volunteers and patients with ID. The level of SGK1 in coronary artery lesion (CAL) group of KD was significantly higher than that in KD patients with normal coronary artery (CAN). SGK1 was reduced in KD after intravenous immunoglobulin (IVIG) treatment. What's more, the decrease of SGK1 was more obviously in the CAL group than in the CAN group. In addition, SGK1 expression in KD was positively correlated with RORC and IL-17A, but not with IL-6.
  
  
  CONCLUSIONS
  SGK1 was up-regulated in CD4⁺ T cells and was positively correlated with RORC and IL-17A in the patients with KD.
authors.affiliation: Institute of Pediatrics Disease, Xi'an Children Hospital, Xi'an 710003, China.
authors.forename: Shouzhen
authors.initials: S
authors.lastname: Wu
authors.affiliation: Department of Pediatrics, Shaanxi Provincial People's Hospital, Xi'an 710068, China.
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Institute of Pediatrics Disease, Xi'an Children Hospital, Xi'an 710003, China.
authors.forename: Nan
authors.initials: N
authors.lastname: Zhou
mesh_terms: D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism*; D002675:Child, Preschool; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology*; D006801:Humans; D017874:Immediate-Early Proteins / Q000235:genetics*; D007223:Infant; D020381:Interleukin-17 / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D009080:Mucocutaneous Lymph Node Syndrome / Q000188:drug therapy / Q000209:etiology / Q000276:immunology*; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000097:blood*; D017346:Protein Serine-Threonine Kinases / Q000235:genetics*; D012333:RNA, Messenger / Q000032:analysis; D058504:Th17 Cells / Q000276:immunology; D015854:Up-Regulation; D000099184:Serum-Glucocorticoid Regulated Kinases
chemical_list: D005938:Glucocorticoids; D017874:Immediate-Early Proteins; D020381:Interleukin-17; D015850:Interleukin-6; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D017346:Protein Serine-Threonine Kinases; D012333:RNA, Messenger; D000099184:Serum-Glucocorticoid Regulated Kinases; C508717:IL17A protein, human; C539900:RORC protein, human