PURPOSE OF REVIEW: Historically, researchers have focused on the role of 
adaptive immunity in lupus pathogenesis; recently, however, there has been 
renewed interest in the contributions of a prototypical innate immune cell - the 
neutrophil.
RECENT FINDINGS: Neutrophil extracellular traps (NETs) are released via a novel 
form of cell death called NETosis. NETs, consisting of a chromatin meshwork 
decorated with antimicrobial peptides, play an important role in the innate 
response to microbial infections. Some lupus patients do not clear NETs 
normally, a phenotype that correlates with disease activity. Further, lupus 
neutrophils - and, in particular, an aberrant subset called low-density 
granulocytes - have an increased propensity to undergo NETosis. Both interferon 
alpha (IFNα) and immune complexes are potential triggers of enhanced NETosis in 
lupus patients.
SUMMARY: NETs are a potent stimulus for IFNα release by plasmacytoid dendritic 
cells, and, as such, may play an important role in propagation of the lupus 
phenotype. NETs can also directly damage tissues - including the endothelium - 
with implications for lupus nephritis and accelerated atherosclerosis. Whether 
aberrant NETosis is sufficient to trigger systemic lupus erythematosus, and 
whether inhibition of NETosis can ameliorate clinical manifestations of lupus, 
are open questions, and will be exciting topics of future research.