Association of Toll-like receptor 2-positive monocytes with coronary artery lesions and treatment nonresponse in Kawasaki disease

Kang, Soo Jung; Kim, Nam Su

Previous studies on TLRs in KD have focused on the feasibility of coronary arteritis animal model in elucidating the pathophysiologic mechanisms involved in CAL development in KD in humans 16) or elevated levels of TLRs in KD regardless of the CAL status 24) . The role of TLR2 expression in CAL development in KD has been studied using a coronary arteritis mouse model induced with LCCWE, and TLR2 was shown to be involved in inducing focal co ronary arteritis 16) . The feasibility of the LCCWE mouse model, in representing the mechanisms of TLR activity in patients with KD, was investigated by Lin et al. 24) , who reported that both patients with KD and LCCWE mouse model developed similar cardiac lesions as well as coronary arteritis and that a similar pattern of cytokine increase was noted, such as elevation in sIL10 and TNFα in the acute phase of KD in both patients with KD and LCCWE mouse model. This report also showed that in both patients with KD before IVIG treatment and LCCWE mouse model, the surface expression of TLR2 on circulating CD14 + monocytes was increased. This agrees with our results that show increased FTLR2% in the CAL (+) group compared to that in the CAL () group. However, in their study, Lin et al. 24) did not investigate the correlation between TLR expression levels and CAL development or IVIG resistance.