Author/Authors :
Moossavi, Maryam Student Research Committee - Birjand University of Medical Sciences, Birjand, Iran , Shojaee, Maryam Department of Biology - Payame Noor University of Mashhad, IR Iran , Mollashahi, Arezoo Department of Biology - Payame Noor University of Esfehan, IR Iran , Poodineh, Jafar Department of Clinical Biochemistry - School of Medicine - Zabol University of Medical Sciences, Zabol, IR Iran , Moossavi, Zahra Shiraz University of Medical Sciences, Shiraz, IR Iran , Alaei, Maryam Department of Clinical Biochemistry - Faculty of Medical Sciences - Tarbiat Modares University, Tehran, IR Iran , Ibrahimi, Mostafa Department of Clinical Biochemistry - Faculty of Medical Sciences - Tarbiat Modares University, Tehran, IR Iran , Mohammadoo Khorasani, Milad Department of Clinical Biochemistry - Faculty of Medical Sciences - Tarbiat Modares University, Tehran, IR Iran
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,
somepolymorphismscan control the expression of interleukins. Consequently, genetic studies can shed lightonour 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.
Keywords :
Polymorphism , Systemic Lupus Erythematosus , Cytokines , Interleukin-1
