Article Abstract

Elucidating new drug targets in psoriasis by gene profiling: an opportunity to be seized

Authors: Mark R. Walter

Abstract

Psoriasis vulgaris (psoriasis) is an autoimmune disease of the skin that affects ~3% of the world’s population (1). It is easily diagnosed by characteristic red colored plaques most often located on the elbows, knees, and scalp. Importantly, psoriasis patients (PP) have shorter lifespans and higher risk of cardiovascular disease, obesity, and diabetes (2). The development of biologics for the treatment of psoriasis is a remarkable success story of translational medicine, which arguably started with the identification of T cell infiltrates in psoriatic lesions ~30 years ago (3,4). The molecular basis of psoriasis continues to be refined and therapeutic approaches in humans now provide critical data to improve our understanding of the disease. For example, the confirmation that psoriasis was a T cell-mediated disease was ultimately established using monoclonal antibodies (mAbs) that broadly eliminated T cells by various mechanisms. Subsequently, IL-23 was found to regulate TH17 and TH22 cell production (IL-23/TH17 axis) and the main cytokines produced by these cells (IL-17 and IL-22) were found in high levels in human psoriatic plaques (4-6).

Refbacks

  • There are currently no refbacks.