Neutrophil extracellular traps (NETs) are extracellular fibrillar networks that concentrate antimicrobial substances at sites of infection and trap microbes, helping to prevent their spread. They are produced by neutrophils in response to infectious pathogens (mainly bacteria and fungi) and inflammatory mediators (e.g., chemokines, cytokines [mainly interferons], complement proteins, and ROS). The extracellular traps consist of a viscous meshwork of nuclear chromatin that binds and concentrates granule proteins such as antimicrobial peptides and enzymes. NET formation starts with ROS-dependent activation of an arginine deaminase that converts arginines to citrulline, leading to chromatin decondensation. Other enzymes that are produced in activated neutrophils, such as MPO and elastase, enter the nucleus and cause further chromatin decondensation, culminating in rupture of the nuclear envelope and release of chromatin. In this process, the nuclei of the neutrophils are lost, leading to death of the cells. NETs have also been detected in the blood during sepsis. The nuclear chromatin in the NETs, which includes histones and associated DNA, has been postulated to be a source of nuclear antigens in systemic autoimmune diseases, particularly lupus, in which individuals react against their own DNA and nucleoproteins.