Author(s): Tue Kruse Rasmussen, Rasmus Otkjær Bak, Thomas Andersen, Anders Dige, Christian Holm, Jacob Giehm Mikkelsen and Bent Deleuran
Systemic lupus erythematosus is clinically and pathologically heterogeneous disease. The pathogenesis of SLE is still unknown but the hallmarks of SLE are autoantibodies directed towards DNA- and RNA-associated molecules and defects in the regulation of apoptosis. These abnormalities result in inflammatory reactions in a range of organs such as the skin, kidneys, eyes and the central nervous system (CNS). SLE patients experience a relapsing disease pattern with flaring of symptoms such as rash, fever, hair loss, tiredness and in severe cases kidney failure and CNS affection. Systemic lupus erythematosus is characterized by both increased apoptosis of leukocytes and defective clearance of apoptotic debris. This increased apoptosis of leukocytes from SLE patients is reflected by their tendency to develop lymphopenias during disease flare. Several groups have studied and replicated this process but no clear cause for the increased apoptosis of lymphocytes has been found.
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