Neutrophils are the most abundant leukocytes in circulation and represent one of 
the first lines of defense against invading pathogens. Neutrophils possess a 
vast arsenal of antimicrobial proteins, which can be released from the cell by a 
death program termed NETosis. Neutrophil extracellular traps (NETs) are web-like 
structures consisting of decondensed chromatin decorated with granular and 
cytosolic proteins. Both exuberant NETosis and impaired clearance of NETs have 
been implicated in the organ damage of autoimmune diseases, such as systemic 
lupus erythematosus (SLE), small vessel vasculitis (SVV), and psoriasis. NETs 
may also represent an important source of modified autoantigens in SLE and SVV. 
Here, we review the autoimmune diseases linked to NETosis, with a focus on how 
modified proteins externalized on NETs may trigger loss of immune tolerance and 
promote organ damage.