title: The T helper type 17/regulatory T cell imbalance in patients with acute Kawasaki disease.
abstract: The study is designed to investigate the changes and roles of T helper type 17/regulatory T cells (Th17/T(reg) ) in the immunological pathogenesis of Kawasaki disease (KD). In addition, we explore the alteration and significance of Th17 cells in patients with intravenous immune globulin-resistant KD. Real-time polymerase chain reaction (PCR) was used to evaluate the mRNA levels of interleukin (IL)-17A/F, retinoic acid-related orphan receptor (ROR)-γt and forkhead box P3 (FoxP3) in CD4-positive cells. The proportions of Th17 cells and CD4(+) CD25(+) FoxP3(high) T(regs) were analysed by flow cytometry. Plasma cytokine [IL-17A, IL-6, IL-23 and transforming growth factor (TGF)-β] concentrations were measured by sandwich enzyme-linked immunosorbent assay. Our data demonstrate that Th17 proportions and expression levels of cytokines (IL-17, IL-6 and IL-23) and transcription factors (IL-17A/F, ROR-γt) were up-regulated significantly, while T(reg) proportions and expression levels of T(reg ) transcription factor (FoxP3) were down-regulated significantly in children with acute KD (P<0·01). Compared with the sensitive group, the Th17 proportions were up-regulated significantly during the acute phase in immune globulin-resistant KD (P < 0·01). The plasma IL-17A, IL-6 and IL-23 concentrations in patients with KD were significantly higher compared with the concentrations in normal controls (NC) and infectious disease (ID). Plasma TGF-β concentrations were markedly lower in the KD group than the NC and ID groups (P < 0·05). These results suggest that Th17/T(reg) cells imbalance exists in the patients with KD. Th17/T cells imbalance may be important factors causing disturbed immunological function and resulting in immunoglobulin-resistant KD.
authors: Shenzhen Institute of Pediatrics, Shenzhen Children Hospital, Chongqing University of Medical Sciences, Shenzhen, China.
authors: S
authors: S
authors: Jia
authors: C
authors: C
authors: Li
authors: G
authors: G
authors: Wang
authors: J
authors: J
authors: Yang
authors: Y
authors: Y
authors: Zu
mesh_terms: D002675:Child, Preschool; D004351:Drug Resistance; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D051858:Forkhead Transcription Factors / Q000097:blood / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use; D007223:Infant; D019410:Interleukin-16 / Q000097:blood; D020381:Interleukin-17 / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D053759:Interleukin-23 / Q000097:blood; D008297:Male; D009080:Mucocutaneous Lymph Node Syndrome / Q000188:drug therapy / Q000276:immunology* / Q000378:metabolism; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000097:blood / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology* / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism
chemical_list: C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D016756:Immunoglobulins, Intravenous; D019410:Interleukin-16; D020381:Interleukin-17; D053759:Interleukin-23; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3