Serum interleukin-17 expression in a group of Egyptian patients with juvenile systemic lupus erythematosus

INTRODUCTION Systemic lupus erythematosus (SLE) is a chronic multi-organ systemic autoimmune disease characterized by autoantibody production to nuclear antigen resulting in inflammation and damage to numerous organs particularly kidneys. It appears in genetically prone individuals and is triggered by illdefined environmental factors. The deposition of autoantibodies occurs in vulnerable vascular beds frequently in skin, joints and renal glomeruli causing local inflammation and tissue destruction that may magnify the autoimmune response creating. Till date the complete understanding of SLE pathogenies is unclear. However, it is well known that dysregulation of B-and T-cell activation will lead to disruption in immune system, and this is considered a key role in SLE pathogenies. In addition, proinflammatory cytokines contribute to the pathogenesis of SLE. These include interleukin (IL)-1 1β, IL-6, IL-17 and tumor necrosis factor (TNF)-α and their levels may correlate with SLE activity. Interleukin-17 (IL-17) is produced by T-helper 17 (Th17) cells and other immunological cells. IL17 consists of six protein members [IL-17A, IL17B, IL17-C, IL-17D, IL-17E , and IL-17F] of which IL-17A and IL-17F are responsible for the activity of Th17 cells in the induction of other cytokines and chemokines. 6,7 IL-17, is a pleiotropic pro-inflammatory cytokine that enhances T-cell priming and stimulates epithelial, endothelial, and fibroblastic cells to produce other multiple proinflammatory mediators such as TNF-α, IL-1β, and IL-6. -17 plays a critical role in innate and adaptive immune systems by promoting Original article