INTRODUCTION
The skin is the second largest organ of the body. It acts as a protective barrier and is a reflection of overall health. This makes the cutaneous conditions different from those affecting internal organs. Skin diseases are often visible to others. Patients with skin diseases suffer due to the disease burden and social stigma associated with these conditions. Psoriasis is a commonly occurring chronic papulo-squamous inflammatory skin disease. It presents with various clinical manifestations and has a wide spectrum of features, which occurs due to the complex interplay of genetic, environmental, and immunological factors. It is known to affect 2%–4% of the population in western countries. Age, geographic location, and genetic background are known to influence the prevalence range. Both genders are equally affected, and they occur universally.1 Psoriasis is known to occur at any age, but it has a bimodal peak of onset, with the first peak occurring between 20 and 30 years and the second between 50 and 60 years.2 It is of importance as it affects the quality of life. Patients with psoriasis often experience anxiety, depression, low self-confidence, and suicidal behavior.3 The pathogenesis of psoriasis is not completely understood despite being studied exclusively.4 The complex interaction between keratinocytes, T-lymphocytes, mast cells, dendritic cells (DCs), and neutrophils is represented by its histopathological changes such as, elongated rete ridges, hyperkeratosis with parakeratosis, Munros’ micro-abscesses, and dilated vessels in the dermal papilla.5 Years of research have led to a description of the pathogenic model of psoriatic plaque formation. Initially, the disease was considered to be an epidermal disorder with many mediators like protein kinase C, cyclic adenosine monophosphate, eicosanoids, phospholipase C, transforming growth factor (TGF)-α having a central role.6 Role of T-cells was recognized and interleukin (IL)-12 and interferon (IFN)-γ were considered key factors driving the pathogenesis of psoriasis during later years.7 Tumor necrosis factor (TNF)-α is important in its pathogenesis and the biological therapies targeting TNF-α revolutionized the treatment of psoriasis vulgaris.8,9 Cytokines of the IL-23/IL-17 axis are extensively studied in pathogenesis of psoriasis.7 Despite availability of many topical and systemic agents, treating psoriasis is often difficult
