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Abstract
Psoriasis is a common chronic condition characterized by thick scaling red plaques which can be either localized or
widespread. The disorder is characterized by spontaneous remission and exacerbations. Over the years, psoriasis occupied the position of one of the most prevalent autoimmune diseases worldwide; it affects approximately 2-3% of the population.
This fact along with its great burden –emotionally and physically- on patients made it the focus of a lot of researches
and investigations. The exact pathogenesis of psoriasis is still a
matter that changes every day with new theories and explanations.
For a long time psoriasis was believed to be a primary keratinocytes hyperproliferation disorder. Recent progress in the understanding of psoriasis has attributed its pathogenesis to the important role of T cells; specifically Th1 and Tc1-although
it cannot be merely explained by T cell role only as mentioned above.
In psoriasis, the initial activation of T-lymphocytes
requires three steps: binding, signal 1 and signal 2. Binding occurs between surface adhesion molecules of both Tlymphocytes and APCs, then additional interactions occur at “signal 1” between TCR on T-cell and MHC I or II on APC, a process that is followed by additional interactions “signal 2”
which, in their absence, T-cells undergo anergy or apoptosis.
The trafficking of T-cells into the skin involves three steps:
rolling, binding and diapedesis. Activated T-cells produce Th-1
cytokines (IL-2, TNF-α, IFN-γ) which, along with chemokines and growth factors, are responsible for the inflammatory infiltrate, vascular changes and the epidermal hyperproliferation present in psoriasis.