• lupus nephritis
• inflammation
• autoimmunity
• autoantibodies
• infections

Systemic lupus erythematosus (SLE) is a prototypic autoimmune disorder affecting multiple organ systems including skin, joint and several internal organs such as kidney, heart or lung. A hallmark of this disease is the development of circulating antibodies against nuclear antigens and immune complex formation. The best-known antibodies are directed against native DNA and are prognostic for development of lupus nephritis. The processes resulting to the cascade of events culminating in the clinical features of SLE are only partially understood and involve among others, defective clearance of apoptotic cells and enhanced DNA damage to ultraviolet irradiation, and netosis1 2 (figure 1). It has also been suggested for a long time that certain microbial triggers could play a role in the onset of SLE, supported by early reports that antibody responses to nucleic acids/nucleoproteins were found in association with certain bacterial infections. More recently, more definitive proof of concept studies using germ-free and reconstituted mice highlighted that intestinal microbiota are able to drive development of systemic autoantibody responses.3 4 However, whether similar processes underlie development of lupus nephritis and anti-DNA antibodies was unclear.