Systemic lupus erythematosus (SLE) is a severe autoimmune disease in which the immune system attacks the body’s own tissues. The disease can affect various organs and primarily occurs in young women. Some patients experience symptoms and have autoantibodies in their blood that are suggestive of SLE, but not enough for the classification of the disease. This early phase is referred to as incomplete SLE (iSLE). About one in five of these patients eventually progress to SLE.
In this thesis of Svenja Henning, differences in both the innate and adaptive immune system were compared between iSLE patients, SLE patients and healthy individuals. In iSLE patients, activity of certain immune signaling molecules (interferons) was elevated in clinically normal-appearing skin and blood. This may lead to sustained immune activation even in early phases of SLE and suggests that the skin is an immune-activated site in both iSLE and SLE.
Additionally, we found elevated levels of neutrophil extracellular traps (NETs) and an increase in low-density granulocytes in both iSLE and SLE patients. These abnormal white blood cells can release their DNA, thereby promoting immune responses against the body’s own tissues. Changes were also observed in B cells that may lead to the production of harmful autoantibodies.
In summary, this thesis shows that the immune system is already dysregulated in iSLE patients. These new insights contribute to a better understanding of how SLE develops and may hopefully aid in the development of early treatments in the future.
