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Official Journal of the Italian Society of Dermatology and Sexually Transmitted Diseases
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,014
Online ISSN 1827-1820
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Somani A. K., Yang M. F., Cooper K. D., McCormick T. S.
Department of Dermatology University Hospitals Case Medical Center/Case Western Reserve University Murdough Family Center for Psoriasis, Cleveland, OH, USA
Psoriasis vulgaris is one of the most common autoimmune skin diseases, afflicting approximately 2-3% of the global population. The disease is characterized by erythematous plaques that constantly shed scale secondary to excessive proliferation of epidermal keratinocytes. Lesions are defined by the presence of infiltrating leukocytes including intraepidermal CD8+ T cells and neutrophils, along with epidermal acanthosis, vascular hyperplasia, and ectasia. Psoriasis is an immune-mediated disease in which genetic-susceptibility alleles and immunological and environmental factors contribute to the chronic inflammatory process incited by the interplay of infiltrating cell types and resident skin cells. There have been significant advances in our understanding of the immunopathogenesis and genetics of the disease process; however, the cause of psoriasis remains unknown and the cure still elusive. Central to the complex interplay of resident skin and immune cells are pro-inflammatory cytokines, chemokines, growth factors, and chemical mediators elaborated by cutaneous cells that direct the disease process. Given the primacy of cytokines that drive cutaneous immune responses and ultimately psoriatic plaque formation, these “pathokines” represent ideal targets for biological therapies. In this article, the crucial effector functions of cytokines in the immunological process that are central to the pathogenesis of psoriasis, and the current treatment modalities that target cytokines will be discussed.