Kawasaki disease is an acute febrile disease in children and many inflammatory cytokines are known to be involved in its pathogenesis. Interleukin-10 (IL-10) is an anti-inflammatory cytokine and previous reports have shown blood IL-10 levels were elevated during the acute phase of Kawasaki disease. In this study, we endeavoured to clarify the effects of IVIG on plasma IL-10 levels and to verify by RT-PCR, using specific primers, whether viral IL-10 or human IL-10 was responsible for high plasma IL-10. T-cells and B-cells were separated using magnetic beads, and IL-10 mRNA expressions were tested in both cell types. The mean plasma IL-10 levels were significantly decreased from 125.037±111.161 pg/ml, before IVIG treatment, to 32.437±54.716 pg/ml, after IVIG treatment, in subjects with Kawasaki disease. The levels of patients before IVIG treatment were significantly higher than those of the acute febrile patients (mean 26.956±13.316 pg/ml) and the normal controls (mean 16.042±5.088 pg/ml). RT-PCR was performed using specific primers to distinguish whether viral IL-10 (BCRF-1) or human IL-10 was produced in Kawasaki disease. Viral IL-10 (BCRF-1) mRNA expression was not detected in any groups and only human IL-10 mRNA transcripts were detected in PBMCs of Kawasaki patients as well as in those of acute febrile patients and normal controls. Human IL-10 mRNA transcripts were detected in both CD3+ T-cells and CD19+ B-cells. Elevated IL-10 levels during the acute phase of Kawasaki disease decreased immediately after IVIG administration, coincidentally with rapid improvement of inflammatory symptoms. Elevated plasma IL-10 in Kawasaki disease was transcripted from the human IL-10 gene and IL-10 mRNA expressions were detected in both T- and B-cells. Therefore, this study suggests that plasma IL-10 levels may be useful in the early identification and discrimination of the acute phase of Kawasaki disease from other febrile diseases. However, IVIG effects on IL-10 production still needs further investigation.