CLEC5A (C-type lectin domain family 5, member A; also known as myeloid DAP12-associating lectin (MDL-1)) Journal of Biomedicine and Biotechnology contains a C-type lectin-like fold similar to the naturalkiller T-cell C-type lectin domains and is associated with a 12-kDa DNAX-activating protein (DAP12) on myeloid cells [12] [13] [14] . Signaling via this complex constitutes a significant activation pathway in myeloid cells and plays an important role in immune defense. Recently, it has been demonstrated that CLEC5A acts as a signaling receptor for proinflammatory cytokine release, and that blockade of CLEC5A-mediated signaling attenuates the production of proinflammatory cytokines by macrophages infected with dengue virus [14] . In contrast, it has been demonstrated that MDL-1 stimulation induces a significant amount of RANTES and macrophage-derived chemokine (MDC) production in cooperation with signaling through TLR in mouse myeloid cells [15] . Furthermore, there is ample evidence that activation of peripheral blood monocytes/macrophages [16] [17] [18] , proinflammatory cytokines [16] , and the RANTES gene play a central role during acute KD [19, 20] . A persistent or increased expression of chemokine genes in the convalescent phase in patients is associated with coronary artery lesions [17, 19] . In addition, infiltration by the cells is notable in affected tissues in autopsy cases and in skin biopsy specimens from KD patients [21] .