Abstract
Chronic plaque psoriasis is a common debilitating skin disease. The identification of the pathogenic role of the TNF/IL-23/TH17 pathway has enabled the development of targeted therapies used in the clinic today. Particularly, TNF inhibitors have become a benchmark for the treatment of numerous chronic inflammatory diseases such as psoriasis. Although being highly effective in psoriasis treatment, anti-TNFs can themselves induce psoriasis-like skin lesions, a side effect called paradoxical psoriasis. In this review, we provide a comprehensive look at the different cellular and molecular players involved in classical plaque psoriasis and contrast its pathogenesis to paradoxical psoriasis, which is clinically similar but immunologically distinct. Classical psoriasis is a T-cell mediated autoimmune disease driven by TNF, characterised by T-cells memory, and a relapsing disease course. In contrast, paradoxical psoriasis is caused by the absence of TNF and represents an ongoing type-I interferon-driven innate inflammation that fails to elicit T-cell autoimmunity and lacks memory T cell-mediated relapses.
Highlights
Psoriasis is a distinctly human, chronic, inflammatory skin disease, affecting 2–3% of the population worldwide, with prevalence varying considerably according to race and geographic location [1]
This review aims to provide a focussed overview of the latest developments in the T-cell and cytokine networks in classical psoriasis, and contrast them to paradoxical psoriasis induced by anti-TNFs, which is clinically similar to psoriasis but immunologically distinct
The psoriatic phenotype was only induced by migration of T-cells into the epidermis and blockade of the epidermal infiltration by T-cells prevented the development of a psoriatic lesion [20]. These findings suggest that intraepidermal T-cells reflect key effector cells in psoriasis
Summary
Chronic plaque psoriasis is a common debilitating skin disease. TNF inhibitors have become a benchmark for the treatment of numerous chronic inflammatory diseases such as psoriasis. Being highly effective in psoriasis treatment, anti-TNFs can themselves induce psoriasis-like skin lesions, a side effect called paradoxical psoriasis. We provide a comprehensive look at the different cellular and molecular players involved in classical plaque psoriasis and contrast its pathogenesis to paradoxical psoriasis, which is clinically similar but immunologically distinct. Classical psoriasis is a Tcell mediated autoimmune disease driven by TNF, characterised by T-cells memory, and a relapsing disease course. Paradoxical psoriasis is caused by the absence of TNF and represents an ongoing type-I interferon-driven innate inflammation that fails to elicit T-cell autoimmunity and lacks memory T cell-mediated relapses
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