الفهرس | Only 14 pages are availabe for public view |
Abstract Psoriasis is a chronic inflammatory skin disease with polygenic predisposition combined with triggering environmental factors. It is a chronic papulosquamous skin disease characterized by complex alterations in epidermal growth and differentiation, and multiple biochemical, immunologic and vascular abnormalities. Autoimmunity is believed to play a central role in the development of PV. The immune response in PV is associated with aberrant lesional expression of IFN-γ, IL-2, and TNF-α. Together with these cytokines, HMGB1 may constitute a proinflammatory loop and may act as an important player in the inflammatory processes in PV. Activated HMGB1 mediates cellular responses including chemotactic cell movement and release of proinflammatory cytokines such as TNF-α, IL-1 β, and IL-6, and effects on various immune cells, such as macrophages, monocytes, T cells, and B cells. With the discovery of HMGB1 as a potent mediator of inflammation and the presence of extranuclear HMGB1 in several inflammatory conditions, investigations of possible beneficial effects of HMGB1-targeted therapies were initiated. Many studies have concluded that HMGB1 is a key player in the pathogenesis of several autoimmune diseases such as R.A, SLE and AA. |