Genetics and adaptive immunity have been the focus of most research in autoimmune diseases, but now there is growing interest regarding involvement of epigenetics and the innate immune response. The report by Hirankarn et al.1 in this issue is quite timely as it provides insights into DNA methylation (epigenetic control) in neutrophils (first responders in the innate response) in lupus patients.

As neutrophils comprise the majority of white blood cells, are part of the innate immune response, and are typically the first immune cells to arrive at an infection site, we should suspect them of having an important role early in an autoimmune episode. Indeed, the recently discovered innate immune response process of NETosis has been proposed as a means by which modified nuclear material can be exposed extracellularly to the adaptive immune system and potentially initiate an autoimmune reaction.2, 3 In NETosis, a neutrophil is stimulated to modify its chromatin and extrude the chromatin as a neutrophil extracellular trap, which binds pathogenic material to facilitate rapid removal by macrophages.4 As this process yields a mixture of pathogenic and nuclear material during an inflammatory reaction, it is important to consider how abnormal epigenetic changes could alter this process.

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