Abstract
Systemic lupus erythematosus (SLE) is a complex multisystemic autoimmune disease with considerable clinical and immunological heterogeneity. Although the exact pathogenetic mechanisms have yet to be elucidated, both genetic and environmental factors are thought to be involved [1]. SLE is characterized by a myriad of immunological aberrations, which can be either the cause or effect of the disease. These abnormalities include aberrant apoptosis and defective clearance of apoptotic materials such as nuclear autoantigens and nucleosomes, as well as immune complexes by macrophages and the complement system [2], increased maturation of myeloid dendritic cells that drive the development of the proinflammatory Th17 cells [3], and defective functions of the regulatory T cells (Tregs) leading to hyperactivity of the helper T cells and autoreactive B cells [4]. The end result is B-cell hyperactivity contributing to increased autoantibody production. Autoantibodies mediate tissue injury by the formation of immune complexes and subsequent complement activation, as well as through the direct mechanism of antibody-mediated cytotoxicity.
Published Version
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