الفهرس 
Systemic Lupus ErythematosusOnly 14 pages are availabe for public view
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Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by autoantibody production, immune complex deposition, and various clinical systemic manifestations that affect various organs. The pathogenesis of SLE involves complex interactions between genetic and environmental factors and the adaptive and innate immune systems. The breakdown of immunologic self-tolerance, that is, the control of self- and non-self-discrimination, results in the development of autoimmune diseases.
Treg cells are a specialized T cell subpopulation capable of controlling and limiting the harmful immune response. Treg cells also prevent the immune response against self-antigens and have a strong suppressive activity under inflammatory conditions .Regulatory T cells subpopulation is believed to play a key role in maintaining peripheral tolerance through the mechanism of controlling circulating autoreactive T cells that have not been removed in the thymus. They are characterized by the constitutive expression of CD25 [interleukin-2 (IL-2) receptor alpha chain], cytotoxic T-lymphocyte antigen 4 (CTLA-4), glucocorticoid induced tumor necrosis factor receptor-related protein (GITR), and transcriptional repressor forkhead box P3 (FoxP3), and a low level or nonexpression of CD127 (IL-7 receptor)
Quantitative and/or qualitative deficiencies of Tregs have been associated with the development of SLE.
This study performed in a total of 75 subjects involving 50 patients and 25 healthy controls with matched age and sex, their ages ranged between 16 – 64 years. They were randomly selected from Menoufia University Hospitals in the duration between May 2016.