Pathophysiology and Molecular Basis of Psoriasis

Psoriasis, a papulosquamous skin disease, is estimated to affect 2% of the global population. Traditionally believed to be a problem largely affecting keratinocytes in the epidermis, psoriasis has recently been identified as one of the most common immune-related diseases. Though this condition may manifest at any life stage, a dual distribution of age was observed, having a peak occurring between the ages of 20 and 30 as well as 50 and 60. Psoriasis possesses a complicated etiology that includes immunologic, hereditary, and systemic/local factors. Psoriasis shows an immense negative impact on human life quality, probably equivalent in comparison to coronary artery disease, type 2 diabetes, depressive disorders, and carcinoma, regardless of the fact that it usually possesses a minor influence on survival. The unregulated development of keratinocytes is the main constraint behind psoriasis, and improper regulation of the immune system serves as a pathophysiological factor. The pathogenesis generally includes the cooperation among several populations for immunocytes along with corresponding transmitting molecules that are: (1) innate immunocytes, which are mediated by antigenic-displaying cells, such as neutrophils, the cells of Langerhans, and natural-killing T lymphoid cells (2) acquired or adaptable immunocytes, which are facilitated by developed CD4+ and CD8+ T lymphocyte residing in the epidermis. The result of such immunological dysfunction leads to inflammation, which causes clinical lesions as well as histopathological inflammation, diagnostic of psoriasis development and perpetuation. The standard of lifestyle in patients has increased with biologic treatments, which focus on the cytokine-mediated pathophysiology of psoriasis. This book chapter will cover the molecular basis and primary pathophysiology of psoriasis.