Abstract
Psoriasis is a recurrent, chronic, immune-mediated, systemic inflammatory disease of the skin, joints, and other organic systems. After atopic dermatitis, chronic stationary psoriasis is the most common inflammatory skin disease, affecting an average of 2–4% of the world’s population. The disease carries a significant burden due to its numerous comorbidities and the major impact on patients’ social and emotional aspects of life. According to current knowledge, psoriasis is a multifactorial disease that occurs in genetically predisposed individuals under various environmental factors, which trigger an immune response disorder with a series of complex inflammatory cascades. The disease is initiated and maintained by mutual interaction of the innate and adaptive immune cells, primarily dendritic cells, T lymphocytes, and keratinocytes, whose leading role alternates at different stages of the disease, consisting mainly in the IL-23/Th17 pathway. Inflammatory events result in consequent epidermal and dermal changes and evolution of the characteristic psoriatic phenotype, respectively. This paper aims to present a comprehensive overview of current knowledge on psoriasis genetic and environmental etiological factors, immunopathogenesis, and the leading cellular and cytokine participants in the inflammatory pathways of this disease.
Highlights
Psoriasis is a chronic, recurrent, immune-mediated, inflammatory skin disease that is characterized by the clinical appearance of sharply demarcated, erythematous papules or plaques covered with silvery-white scales [1]
The remaining nonclassical lymphocytes, which contribute to the pathogenesis of the disease by releasing IL-17, TNF-α, IFN-γ, and other inflammatory cytokines and chemokines, are natural killer (NK) and Natural killer T-cells (NKTs) cells, innate lymphoid cells (ILCs) cells, and the so-called mucosal-associated invariant T (MAIT) lymphocytes [63,69]
The innate immunity cytokine, TNF-α, is elevated in patients’ serum and psoriatic skin [104]. It is produced by keratinocytes, macrophages, Dendritic cells (DCs), and T lymphocytes, and its receptors, which are present in practically all body cells, activate NF-κB, MAPK, and JNK pathways [111]
Summary
Recurrent, immune-mediated, inflammatory skin disease that is characterized by the clinical appearance of sharply demarcated, erythematous papules or plaques covered with silvery-white scales [1]. After atopic dermatitis, the most common inflammatory skin disease, whose incidence has been slightly increasing in the last three decades [2]. Psoriasis affects about 2–4% of the world’s population [2] People of both sexes suffer while the disease is present mainly in adults and most often occurs in two age groups, between 20 and 30 years and 50 and 60 years [2]. The same mechanism contributes to the development of concomitant diseases, where 73% of patients, especially those with severe psoriasis, have at least one comorbidity [6]. The most common specific causes of death in psoriasis patients are cardiovascular incidents followed by infections, malignancies, liver, kidney, respiratory, and digestive system diseases [18,19]. According to today’s knowledge, psoriasis is a multifactorial disease caused by the interaction of genetic and environmental factors [20]
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