In vitro stimulation of TNFα-primed-neutrophils by chimeric anti-human PR3 mAbs or purified IgG from GPA patients (IgG GPA) induces their auto-immune activation leading to ROS production, protease release by degranulation and adhesion molecules upregulation (10, 12, 13). Here, PRTN3 is linked to granulomatosis with polyangiitis.