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. © 2013 Blackwell Publishing Ltd.
CITATION STYLE
Ge, X., Li, C. R., Yang, J., & Wang, G. B. (2013). Aberrantly Decreased Levels of NKG2D Expression in Children with Kawasaki Disease. Scandinavian Journal of Immunology, 77(5), 389–397. https://doi.org/10.1111/sji.12022
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