Psoriasis is a chronic autoimmune skin disorder which involves complex interactions
between genes, keratinocytes, T-cells and inflammatory cells. It affects 2-3% population worldwide.
Molecular biology and cellular immunology of psoriasis, when linked with biotechnology
and genetic studies can help researchers to understand the pathophysiology of psoriasis. T-cells
activation, keratinocyte hyperproliferation, and angiogenesis are the core mechanisms entailed in
the development of psoriasis lesion. Investigators are trying to overcome the challenges of complex
pathophysiology pathways involved in this disorder. The different possible hypotheses for its
pathophysiology such as growth factors, enzymes, inflammation, and genetic factors mediated
pathophysiology have been described in the present review paper in detail. Clinically available
drugs only control the symptoms of psoriasis but are not effective for the treatment of the disorder
completely and are also associated with some side effects such as itching, renal disorders, hematologic,
nonmelanoma skin cancer, pulmonary, gastrointestinal toxicity, etc. This paper made an
effort to understand the pathophysiological targets, discuss the research done so far and the treatments
available for the effective management of psoriasis.