In this regard, recent evidence suggests that some NET proteins (eg, LL37, HMGB1) promote the activation of professional antigen-presenting cells by facilitating antigen uptake, interaction with endosomal Toll Like Receptor (TLR) and the release of type-I Interferon (IFN) and other proinflammatory cytokines as in the case of plasmacytoid DCs in SLE.42, 43 Similarly, in autoimmune vasculitis, NETs are highly immunogenic and mediate the transfer of cytoplasmic neutrophil antigens to myeloid dendritic cells, favouring the formation of anti-neutrophil cytoplasmic antibodies.44 This evidence concerns the gene IFNA1 and autoimmune vasculitis.