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    Place in therapy of anti-IL-17 and 23 in psoriasis according to the severity of comorbidities: a focus on cardiovascular disease and metabolic syndrome

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    Introduction Psoriasis is an inflammatory disease nowadays considered not only as a cutaneous but as a systemic disease. Among the numerous comorbidities, psoriatic arthritis (PsA), depression, obesity, and cardiovascular disease (CVD) are considered the most frequent. In addition, metabolic syndrome (MetS), which involves hypertension, dyslipidemia, obesity, and atherosclerosis, has presented a higher prevalence in recent years, especially in psoriatic patients. Areas covered The mechanism linking anti-tumor necrosis factor (TNF) to MetS and CVD has been widely explained, while there are unknowns about inhibitors of interleukin (IL)-17 and -23. Considering the growing incidence of CVD in the world's population and in particular the strict correlation in patients with psoriasis, it is important to identify therapeutic options able to avoid a negative impact on patients with both conditions. The aim of this paper is to perform a review of the scientific literature with a focus on the pathogenetic mechanism linking psoriasis to CVD and MetS. Expert opinion The scientific evidence currently available allows us to consider and support the use of anti-IL-17 and anti-IL-23 as a first-line therapy choice in psoriatic patients with high risk of CVDs or MetS

    Mechanism of action of extracorporeal photochemotherapy in chronic graft-versus-host disease

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    Chronic graft-versus-host disease (GvHD) affects 50% of long-term bone marrow transplant sur- vivors and remains a cause of major long-term morbidity in these patients despite aggressive therapy. Extracorporeal photochemotherapy (ECP), considered as an effective treatment for patients with erythrodermic cutaneous T-cell lymphoma (CTCL), has recently been used successfully in the treatment of GvHD. One of the most intriguing aspects of ECP is its ability to induce two apparently opposite effects: activation of the immune system against neoplastic cells (as in CTCL) and down- regulation of the activity of T-cell clones in autoimmune diseases (as in systemic sclerosis, systemic lupus erythematosus and pemphigus vulgaris) and autoallogeneic immune responses (as in GvHD and allograft rejection). Only a better and more complete understanding of the various mechanisms involved will enable this interesting new therapy to be made more effective and selective
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