BACKGROUND: The aim of this study was to investigate whether T-cell activation is involved in the pathogenesis of Kawasaki disease (KD) resistant to intravenous immunoglobulin (IVIG) treatment. METHODS: Serum samples were obtained from 27 patients who fulfilled the diagnostic criteria for KD. These 27 patients were divided into three groups according to their responses to IVIG: Group A, nine patients who showed no response to either initial IVIG or additional IVIG; Group B, six patients who did not respond to initial IVIG but did respond to additional IVIG; Group C, 12 patients who responded to initial IVIG. Serum samples were obtained before and after initial IVIG. Using a commercial chemiluminescence enzyme immunoassay, we examined the serum levels of two cytokines related to T-cell activation and the severity of inflammation: soluble interleukin-2 receptor and interleukin-6. RESULTS: There were no significant differences in the serum levels of the two cytokines before initial IVIG among the three groups, but significant intergroup differences were evident after initial IVIG in the serum levels of soluble interleukin-2 receptor (P < 0.01, Group A > C) and interleukin-6 (P < 0.01, Group A > B > C). CONCLUSIONS: Our results show that marker of T-cell activation is elevated most markedly in KD patients resistant to both initial and additional IVIG, and suggest that T cells may be activated in refractory KD.
BACKGROUND: The aim of this study was to investigate whether T-cell activation is involved in the pathogenesis of Kawasaki disease (KD) resistant to intravenous immunoglobulin (IVIG) treatment. METHODS: Serum samples were obtained from 27 patients who fulfilled the diagnostic criteria for KD. These 27 patients were divided into three groups according to their responses to IVIG: Group A, nine patients who showed no response to either initial IVIG or additional IVIG; Group B, six patients who did not respond to initial IVIG but did respond to additional IVIG; Group C, 12 patients who responded to initial IVIG. Serum samples were obtained before and after initial IVIG. Using a commercial chemiluminescence enzyme immunoassay, we examined the serum levels of two cytokines related to T-cell activation and the severity of inflammation: soluble interleukin-2 receptor and interleukin-6. RESULTS: There were no significant differences in the serum levels of the two cytokines before initial IVIG among the three groups, but significant intergroup differences were evident after initial IVIG in the serum levels of soluble interleukin-2 receptor (P < 0.01, Group A > C) and interleukin-6 (P < 0.01, Group A > B > C). CONCLUSIONS: Our results show that marker of T-cell activation is elevated most markedly in KDpatients resistant to both initial and additional IVIG, and suggest that T cells may be activated in refractory KD.