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Abstract
: Systemic Lupus Erythematosus (SLE) is a chronic human autoimmune disease, which is characterized by increased activity of B cells and production of antibodies against tissue antigens. It engages many tissues and organs, including joints, kidneys, heart, and the nervous system. Although the exact pathogenesis of SLE remains to be elucidated, it is suggested that genetic background plays a paramount role in SLE etiology. Increasing evidence is indicating an important role for interleukins in progression of SLE. Interleukins are a group of cytokines secreted by T helper cells, monocytes, macrophages, and B cells, which are involved in growth and differentiation of T and B cells. The expression level of interleukins is influenced greatly by genetic composition. Therefore, some polymorphisms can control the expression of interleukins. Consequently, genetic studies can shed light on our understanding of SLE nature. Therefore, in the present study, the researchers reviewed the roles of eight key interleukin polymorphisms and their effects on SLE pathogenic.
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