Research in practice: Disturbance in intracellular nucleic acid metabolism promotes lupus erythematosus.

Lupus erythematosus (LE) is an autoimmune disease with a broad spectrum of cutaneous manifestations. It is characterized by a loss of tolerance to nuclear antigens, including endogenous nucleic acids, autoantibody formation and upregulation of the type I interferon pathway. This can be induced by an immune response to unrestricted extracellular self-antigens. In addition, the molecular characterization of rare monogenic subtypes of LE has revealed insights into the role of cell-intrinsic sensing of endogenous self-nucleic acids in inducing a type I interferon response. This pathway can also initiate and sustain LE. The enhanced understanding of innate and adaptive immune responses in LE is a prerequisite for the development of more targeted therapies.