Autoantibodies in systemic lupus erythematosus

Stephen D. Marks, Kjell Tullus

Systemic lupus erythematosus (SLE) is a multifactorial disorder with multigenic inheritance and various environmental factors implicated in its aetiopathogenesis. Despite the multiple mechanisms involved in the aetiology of SLE being elusive, recent studies have made progress in our understanding of the pathogenic mechanisms via abnormal regulation of cell-mediated and humoral immunity that lead to tissue damage. The heterogeneity of the clinical manifestations probably reflects the complexity of the disease pathogenesis itself. The immune system in SLE is characterised by a complex interplay between overactive B cells, abnormally activated T cells and antigen-presenting cells. This interplay leads to the production of an array of inflammatory cytokines, apoptotic cells, diverse autoantibodies and immune complexes that in turn activate effector cells and the complement system, leading to tissue injury and damage which are the hallmarks of the clinical manifestations. SLE patients have dysregulation of inflammatory cytokines, chemokines and immune response-related genes, as well as of the genes involved in apoptosis, signal transduction and the cell cycle.