Expression of CD180, a toll-like receptor homologue, is up-regulated in children with Kawasaki disease

Kawasaki disease (KD) is an acute febrile illness in childhood characterized by the fort-nation of aneurysms in coronary arteries. It is believed that KD is caused by infectious agents because of its epidemic waves and high incidence of familial occurrence. Because an increase in the levels and dysfunction of B cells in peripheral blood was reported in KID, we investigated the expression of cluster of differentiation 180 (CD 180), a toll-like receptor homologue, in the B cells of children with KD, and in those with bacterial or viral infections. The percentages of CD 180 positive B cells were significantly higher in children with KID or viral infections than in those with bacterial infections or in healthy controls. When the expression levels of CD 180 were compared by using the mean fluorescent intensity ratio of patients to healthy controls, the level of CD180 expression was also significantly up-regulated in children with KD or viral infections. To clarify the effect of viral infection on the expression of CD 180, B cells were stimulated with poly inosinic-cytidyric acid [poly(IC)], a synthetic double-stranded RNA. Poly(IC) clearly enhance CD180 expression in B cells in vitro, both at the protein and messenger RNA levels. These results suggest that similar mechanisms may be involved in the up-regulation of B cell CD 180 expression in patients with either KD or viral infections.