Fig 6. Hypothetical role of decreased IL6 signaling in the persistence of vascular inflammation in acute KD.

The TLR6 variants associated with KD are predicted to yield lower levels of NFKB upon stimulation, thus resulting in lower levels of IL6. During vascular inflammation, neutrophil apoptosis is associated with shedding of the soluble IL6R-IL6 complex, which binds to gp130 on endothelial cells. This stimulates a signaling pathway that switches the adhesion molecule and chemokine profile to one that favors attraction of monocytes to the vessel wall with subsequent downregulation of vascular inflammation. In KD, lower levels of IL6 may lead to persistence of neutrophil recruitment to the vessel wall and prolonged inflammation.