Systemic lupus erythematosus (SLE) is a complex and heterogeneous autoimmune disease of unclear etiology. However, it is widely accepted that the pathogenesis of SLE has a strong genetic component. Over the past 30 years, studies in mice and humans have uncovered many genes that are thought to be implicated in SLE development. Despite its heterogeneity, SLE is characterized primarily by high titers of autoantibodies to nuclear and cytoplasmic antigens. Over the years, this feature has led investigators to conclude that SLE develops, in part, as a consequence of a generalized loss of immune tolerance. This article reviews the genetics of SLE in the context of a breach of immune tolerance.
ASJC Scopus subject areas
- Immunology and Allergy