title: Aberrantly decreased levels of NKG2D expression in children with kawasaki disease.
abstract: This study is designed to investigate the changes of NKG2D expression on CD8(+) T cells and CD3(-) CD56(+) NK cells in Kawasaki disease (KD). NKG2D/NKG2A expression on CD3(-) CD56(+) NK cells and CD8(+) T lymphocytes, and NKG2D ligands such as major histocompatibility complex I chain-related molecules A(MICA) and UL-16-binding proteins (ULBP-1) expression on CD14(+) mononuclear cells (MC) were analysed by flow cytometry in patients with KD. Real-time polymerase chain reaction (PCR) was used to evaluate the mRNA levels of interleukin (IL)-1β, IL-6 and tumour necrosis factor (TNF)-α in CD14(+) cells. Plasma cytokine [IL-7, IL-12, IL-15, interferon (IFN)-γ and transforming growth factor (TGF)-β] concentrations were measured by ELISA. The levels of NKG2D on NK cells and CD8(+) T cells expression in acute phase of KD were significantly lower than those in normal controls (P < 0.05), and the levels of NKG2D expression in the patients with coronary artery lesion (KD-CAL(+) ) were lower than those in patients with KD-CAL(-) . There was an upregulated tendency after treatment with IVIG. We found higher expression levels of proinflammatory cytokines from MC, such as IL-1β, IL-6 and TNF-α in patients with KD compared with the healthy controls (P < 0.05). The concentrations of IL-7 and IL-15 were significantly decreased in acute phase of KD (P < 0.05) and to some extent elevated after therapy with IVIG (P < 0.05), while antagonistic cytokines like IFN-γ were increased in acute phase of KD (P < 0.05) and reduced after therapy with IVIG (P < 0.05). These results suggest that aberrantly decreased levels of NKG2D expression on NK cells and CD8(+) T cells might be one of the factors led to disturbed immunological function in patients with KD. Cytokines milieu could be important factors causing reduced expression of NKG2D.
authors.affiliation: Shenzhen Institute of Pediatrics, Shenzhen Children Hospital, Zunyi Medical College, Shenzhen 518026, China.
authors.forename: X
authors.initials: X
authors.lastname: Ge
authors.forename: C-R
authors.initials: CR
authors.lastname: Li
authors.forename: J
authors.initials: J
authors.lastname: Yang
authors.forename: G-B
authors.initials: GB
authors.lastname: Wang
mesh_terms: D019002:CD56 Antigen / Q000276:immunology / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D002675:Child, Preschool; D003331:Coronary Vessels / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D016207:Cytokines / Q000097:blood / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D058851:GPI-Linked Proteins; D015870:Gene Expression / Q000276:immunology; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000276:immunology / Q000627:therapeutic use; D007223:Infant; D053583:Interleukin-1beta / Q000235:genetics; D015850:Interleukin-6 / Q000235:genetics; D047908:Intracellular Signaling Peptides and Proteins; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism; D018950:Lipopolysaccharide Receptors; D008297:Male; D009080:Mucocutaneous Lymph Node Syndrome / Q000097:blood / Q000188:drug therapy / Q000276:immunology*; D055655:NK Cell Lectin-Like Receptor Subfamily K / Q000276:immunology* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D019002:CD56 Antigen; D016207:Cytokines; D058851:GPI-Linked Proteins; D016756:Immunoglobulins, Intravenous; D053583:Interleukin-1beta; D015850:Interleukin-6; D047908:Intracellular Signaling Peptides and Proteins; C527085:KLRK1 protein, human; D018950:Lipopolysaccharide Receptors; D055655:NK Cell Lectin-Like Receptor Subfamily K; D014409:Tumor Necrosis Factor-alpha; C423231:ULBP1 protein, human