Model of the systemic lupus erythematosus pathogenesis based on an autoimmune response to mitochondrial components

Abstract

Systemic lupus erythematosus (SLE) manifests itself in the form of damage to various organs as a result of an autoimmune reaction to the organism's own molecules. Understanding the processes leading to the activation of the autoimmune response, as well as identifying potential autoantigens and their role in the pathogenesis of SIE, is an important task for understanding the mechanisms underlying the pathogenesis of SLE. Here we describe a model of SLE pathogenesis in which the induction of an autoimmune response is based on mitochondrial antigens. In addition to options for initiating an autoimmune response involving mitochondrial components, the model describes the role of pathways and immune cells of these pathways of adaptive immunity in SLE, as well as factors leading to the development of chronic inflammation in SLE. The creation of such models is important for a better understanding of the pathogenesis of SLE, as well as the identification of new therapeutic targets for this disease.