Assessment of IL- 36 gamma in the Sera of Psoriatic Patients

Abstract

Psoriasis is a chronic inflammatory skin disease that is characterized by disfiguring, scaling and erythematous plaques that may be itchy. Although it is thought to be a benign dermatological condition with few serious complications, moderate-to-severe psoriasis is considered a multisystem disease. Psoriasis can be both emotionally and physically debilitating and impact on quality of life significantly. Psoriasis is a genetically determined disease mainly driven by abnormal differentiation secondary to activation of T- cells or antigen presenting cells which in turn release various cytokines and chemokines that signal keratinocytes to hyperproliferation . Psoriasis is an immune-mediated skin disease where the T cell plays a pivotal role in the pathogenesis of the disease. The critical steps involved in the pathogenesis include Langerhans cell activation and maturation by antigens in the skin, activation of the T cell by mature Langerhans cells, differentiation and expansion of T cells within the lymph nodes, trafficking of activated T cells from the lymph node to the skin and the subsequent release of cytokines. Keratinocytes are known to play a crucial in the inflammatory response by producing a panel of pro-inflammatory cytokines and cemokines that not only induce cellular infiltration but can also influence antigen –presenting cell mediated T lymphocytes cytokines profile.These cytokines are responsible for epidermal and vascular hyper proliferation and pro-inflammatory effects. The immune effector cells produce pro-inflammatory cytokines such as tumour necrosis factor α (TNF-α), interferon γ (IFN-γ), interleukin-17 (IL-17), IL-22, IL-23 and IL-1β.