Psoriasis

Abstract

Psoriasis is a chronic, immune-mediated disorder with cutaneous and systemic manifestations and substantial negative effects on patient quality of life. Psoriasis has a strong, albeit polygenic, genetic basis. Whereas approximately half of the accountable genetic effect of psoriasis maps to the major histocompatibility complex, >70 other loci have been identified, many of which implicate nuclear factor-κB, interferon signalling and the IL-23-IL-23 receptor axis. Psoriasis pathophysiology is characterized by abnormal keratinocyte proliferation and immune cell infiltration in the dermis and epidermis involving the innate and adaptive immune systems, with important roles for dendritic cells and T cells, among other cells. Frequent comorbidities are rheumatological and cardiovascular in nature, in particular, psoriatic arthritis. Current treatments for psoriasis include topical agents, photo-based therapies, traditional systemic drugs and biologic agents. Treatments can be used in combination or as monotherapy. Biologic therapies that target specific disease mediators have become a mainstay in the treatment of moderate-to-severe disease, whereas advances in the treatment of mild-to-moderate disease have been limited.

Knockdown of lncRNA MIR31HG inhibits cell proliferation in human HaCaT keratinocytes

“…In order to investigate whether the expression of MIR31HG is dependent on NF-κB activation, we stimulated HaCaT keratinocytes with IL-17A, IL-22, TNF-α and IL-1α. In psoriasis, pro-inflammatory cytokines including IL-17A, IL-22, TNF-α and IL-1α may contribute to the pathophysiology of the disease [2, 19]. IL-17A, IL-22, TNF-α and IL-1α have been reported to be able to activate NF-κB signaling [20, 21].…”

“…Psoriasis is thought to be initiated by complex interactions between genetic and environmental factors [2]. Psoriasis lesions are characterized by epidermal hyperproliferation and aberrant differentiation of keratinocytes and infiltration of inflammatory cells into the dermis and epidermis, which manifests clinically in the thickening and scaling of skin lesions [3].…”

Message in a Bottle: Dialog between Intestine and Skin Modulated by Probiotics

“…The hyperactivity of different cell populations in the SIS, like keratinocytes, DC and specific T-cells, is present in different skin conditions, like psoriasis [29], atopic eczema (AE) [30] and contact dermatitis (CD) [31,32]. …”

Psoriasis: implication to disease and therapeutic strategies, with an emphasis on drug delivery approaches

“…Psoriasis may occur at any age but is more prevalent in the age group of 18–39 years . The onset of psoriasis depends on genetic and environmental factors . Plaque psoriasis is the most common form of the disease and is manifested by raised thick silvery white dead skin cells built up on red patches over skin .…”

“…Psoriasis is mainly an autoimmune disease which is attributed to upregulate the release of proinflammatory mediators like cytokines and chemokines from immune‐associated cells like keratinocytes resulting in hyperproliferation of the epidermis . Psoriasis can be manifested by various phenotypes and is classified in different types, such as plaque psoriasis or psoriasis vulgaris, inverse psoriasis (intertriginous psoriasis), guttate psoriasis, pustular psoriasis, and erythrodermic psoriasis …”