SLE patients have a characteristic increase in the numbers of immature, low-density neutrophils (LDNs) in their peripheral blood,[23] and these SLE-derived LDNs adopt an activated phenotype with augmented production of type I interferon (IFN), Tumor necrosis factor alpha (TNFα) and IFNγ which contribute to disease pathogenesis. This evidence concerns the gene IFNA1 and systemic lupus erythematosus.