Hypothetical model of inhibition of IC-mediated, NO-induced apoptotic pathway in HUVECs by decoy FcγR-Igs.

<p>Circulating ICs deposits in the blood vessels during IC-mediated inflammatory disorders. Effector cells upon binding to the IC get activated. These cells result in the secretion of pro-inflammatory factors like cytokines and toxic superoxide radicals such as nitric oxide in copious amounts. Nitric oxide ability to interact with cellular components in the endothelium results in triggering apoptotic signaling pathway and subsequently cell death and tissue damage. Decoy FcγR-Igs competes with cell surface FcγRs expressed on effector cells and block the access to the ICs deposits in various organs including blood vessels. This will eventually inhibit effector cell mediated endothelial inflammation and damage observed in autoimmune vasculitis.