RNA-binding proteins in autoimmunity: From genetics to molecular biology

Autoimmune diseases (ADs) are chronic pathologies generated by the loss of immune tolerance to the body's own cells and tissues. There is growing recognition that RNA-binding proteins (RBPs) critically govern immunity in healthy and pathological conditions by modulating gene expression post-transcriptionally at all levels: nuclear mRNA splicing and modification, export to the cytoplasm, as well as cytoplasmic mRNA transport, storage, editing, stability, and translation. Despite enormous efforts to identify new therapies for ADs, definitive solutions are not yet available in many instances. Recognizing that many ADs have a strong genetic component, we have explored connections between the molecular biology and the genetics of RBPs in ADs. Here, we review the genetics and molecular biology of RBPs in four major ADs, multiple sclerosis (MS), type 1 diabetes mellitus (T1D), systemic lupus erythematosus (SLE), and rheumatoid arthritis (RA). We anticipate that gaining insights into the genetics and biology of ADs can facilitate the discovery of new therapies.This article is categorized under:RNA in Disease and Development > RNA in Disease

Automated summary

Autoimmune diseases are caused by the immune system's loss of tolerance to the body's own cells and tissues. RNA-binding proteins play a critical role in regulating immunity by modulating gene expression post-transcriptionally. This review explores the connection between the genetics and molecular biology of RNA-binding proteins in multiple sclerosis, type 1 diabetes mellitus, systemic lupus erythematosus, and rheumatoid arthritis. Understanding the genetics and biology of autoimmune diseases can lead to the discovery of new therapies.