Molecular pathogenesis of SLE

Excerpt

Systemic lupus erythematosus (SLE) is an autoimmune disease with extremely diverse and variable clinical manifestations associated with mucocutaneous, joint, renal, cardiovascular, gastrointestinal, liver, pleural, pulmonary, spleen, lymph node, hematological, and central nervous system involvement [1]. Much of the pathology can be induced by continuously produced autoantibodies. Types of autoantibodies detected in sera from patients with SLE are extremely diverse, mainly including antibodies to nuclear components such as DNA, RNA, histones and non-histone proteins, varieties of serum proteins, and cellular antigens particularly of hematopoietic cell origin. Deposition of immune complexes or self-associating complexes formed by some of the autoantibodies causes chronic inflammatory injury in a variety of tissues, and cytotoxic effects of autoantibodies cause hematopoietic and immune cell abnormalities in the peripheral blood and lymphoid tissues. …