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Intravenous immunoglobulin Furusho et al.1) first administered high-dose intravenous immunoglobulin (IVIG) to patients with Kawasaki disease (KD) in the early 1980s. This trial was inspired by the report that high-dose IVIG therapy was very effective for idiopathic thrombocytopenic purpura2) and that its potential mechanism of action was immunomodulation. At that time, Furusho et al.1) suggested that high-dose IVIG had an anti-inflammatory effect in KD to prevent coronary aneurysm (CAA) formation. To date, there have been several hypotheses but little concrete data on the mechanism of action of IVIG in KD. IVIG could interact with many different parts of the immune and vascular systems to downregulate inflammation. Possible interactions of IVIG with elements of the immune system include those with macrophages/monocytes, dendritic cells (DCs), antibodies, T cells, neutrophils, and natural killer (NK) cells.3-6) The changes following IVIG administration in patients with KD have largely been explained, although detailed mechanisms of action are lacking. These changes include a reduction in the levels of cytokines and chemokines; decreased numbers of circulating cluster of differentiation (CD) 14+ monocyte/macrophages, neutrophils and activated T cells; increased numbers of circulating NK cells; and changes in lymphocyte subsets.3)

korean circulation journal

The Efficacy and Safety of High-Dose Intravenous Immunoglobulin in the Treatment of Kawasaki Disease: How Can We Predict Resistance to Intravenous Immunoglobulin Treatment of Kawasaki Disease?