Native alpha-1 antitrypsin can inhibit PR3/anti-PR3 interaction and genes activation/ROS production in cANCA stimulated granulocytes.
Poor inhibition properties of polymerized A1AT are probably caused by loss of antiprotease activity by polymerized form of protein.
Inhibition of cANCA mediated neutrophil activation by alpha-1 antitrypsin is connected with enzymatic activity of plasma expressed proteinase-3.