Psoriasis is a common immune-mediated chronic, non-contagious skin disease which frequently affects the knees, elbows, scalp, hands, feet and lower back. In the case of this auto-immune disease, faulty signals are sent to growing skin cells. Their growth speeds up resulting in increased skin cells or thickening epidermis. As a result of the increase in skin cells, the size of blood vessels also increases as blood supply increases to nourish those cells. At the surface, these skin cells pile up. Dead cells create a white, flaky layer over the patch of inflamed skin.

The disease is defined by a series of linked cellular changes in the skin: hyperplasia of epidermal keratinocytes, vascular hyperplasia and ectasia, and infiltration of T lymphocytes, neutrophils, and other types of leukocyte in affected skin. T lymphocytes are the principal contributors to this autoimmune disease and new biological therapies that target T cells are entering routine clinical practice. Similarly, rapid progress has been made towards dissecting cellular and molecular pathways of inflammation that contribute to disease pathogenesis.

What researchers are currently using:

Methodologies currently in practice include the traditional flow chamber system together with standard well plate, fluorescent readers, protein-antibody interactions, immunoassays and additional procedures allow discrete dissection of the pathogenesis of psoriasis.