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

Abstract

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 typeI 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 typeI 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.