DO OXIDATIVE STRESS AND TOLL-LIKE RECEPTOR ACTIVATION INDUCE NETOSIS IN HUMAN MONOCYTES? FUNCTIONAL CONSEQUENCES ON PRO-THROMBOTIC EVENTS) A SYSTEMATIC REVIEW

Abstract

NETosis occurs during the primary innate immune response to antigens or endothelial damage and is One of the characteristic immune mechanisms related to neutrophils. A component of extracellular neutrophil traps (NETs) activates the pathways for platelet adhesion, allowing complexes of NET fibrin/thrombin to form. These complexes are some of the best pathogen-trapping pathways within the innate immune system, but excessive NETosis can induce blockage of the arteries and, therefore, can result in serious cardiovascular disorders (CVDs) or even cancer. It has been demonstrated in recent research that spreading and tissue-specific monocytes exhibit NETosis in reply to antigens. There are a number of processes that can instigate NETosis, such as the selective proteolysis of toll-like receptors (TLRs) and oxidative stress resulting from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, although the precise pathophysiology is not known.