IL-5 switches the B-cell immunoglobulin to IgA and activates eosinophils.30,31 IgA is considered to be the mediating factor in IgA vasculitis.1 Namgoong et al10 found that eosinophil cationic protein (ECP) and soluble IL-2 receptor levels were significantly higher in patients with IgA vasculitis than in a control group, indicating that T-cell and eosinophil activation were involved in the pathogenesis of IgA vasculitis. This evidence concerns the gene RNASE3 and Henoch-Schoenlein purpura.