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      Plasma Levels of Interleukins 36α, 36β, and 37 in Patients with Psoriasis and Their Correlation with Disease Activity Parameters

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          Abstract

          Psoriasis is a chronic, proliferative, inflammatory skin disease characterised by skin lesions and systemic symptoms. Numerous cytokines are produced in psoriasis as a result of inflammation. The aim of this study was to examine the plasma concentrations of IL-36α, IL-36β, and IL-37 in psoriasis and their correlations with disease activity parameters. This study recruited 84 individuals, 53 with plaque-type psoriasis and 31 healthy controls. The plaque type of psoriasis is the most common type and is typically characterized by circular-to-oval red plaques distributed over body surfaces of the extremities and scalp. In patients with psoriasis, we observed statistically significantly decreased plasma concentrations of IL-36β and IL-37. The concentrations of IL-36α were increased in comparison with control group. The plasma concentrations of IL-36α and IL-36β were statistically significantly correlated with all tested parameters of disease activity: the Psoriasis Activity Severity Index, Dermatology Life Quality Index, and Body Surface Area Index. There were no statistically significant correlations between plasma levels of IL-37 and the tested parameters of disease activity. These results indicate a role of IL36α, IL-36β, and IL-37 in the pathogenesis of psoriasis.

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          Most cited references52

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          Pathogenesis and clinical features of psoriasis.

          Psoriasis, a papulosquamous skin disease, was originally thought of as a disorder primarily of epidermal keratinocytes, but is now recognised as one of the commonest immune-mediated disorders. Tumour necrosis factor alpha, dendritic cells, and T-cells all contribute substantially to its pathogenesis. In early-onset psoriasis (beginning before age 40 years), carriage of HLA-Cw6 and environmental triggers, such as beta-haemolytic streptococcal infections, are major determinants of disease expression. Moreover, at least nine chromosomal psoriasis susceptibility loci have been identified. Several clinical phenotypes of psoriasis are recognised, with chronic plaque (psoriasis vulgaris) accounting for 90% of cases. Comorbidities of psoriasis are attracting interest, and include impairment of quality of life and associated depressive illness, cardiovascular disease, and a seronegative arthritis known as psoriatic arthritis. A more complete understanding of underlying pathomechanisms is leading to new treatments, which will be discussed in the second part of this Series.
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            Inter-regulation of Th17 cytokines and the IL-36 cytokines in vitro and in vivo: implications in psoriasis pathogenesis.

            Accumulating evidence indicates that IL-1 family members and Th17 cytokines have a pathogenic role in psoriasis. We investigated the regulatory interactions of the IL-1-like IL-36 cytokine family and the Th17 cytokines in the context of skin inflammation. We observed increased gene expression of all three IL-36 cytokines in a Th17-dominant psoriasis-like animal model. The induction was downregulated by neutralizing IL-22. Expression of the IL-36s was also induced in cultured primary human keratinocytes (KC) by IL-17A and tumor necrosis factor (TNF)-α, and IL-22 synergized with IL-17A and TNF-α. Furthermore, the IL-36s directly induced their own expression and the production of proinflammatory mediators (TNF-α, IL-6, IL-8) in KC. These functions were markedly enhanced with the addition of IL-17A or TNF-α to the cultures. Similarly, IL-36α and IL-36β augmented IL-17A-mediated induction of antibacterial peptides. Finally, we show that the increased gene expression of IL-36 correlated with Th17 cytokines in the lesions of psoriatic patients. Our results indicate that the IL-36 cytokines are not only regulated by Th17 cytokines, but that they themselves can regulate the expression and enhance the function of Th17 cytokines. We propose that a feedback loop between the IL-36 and Th17 cytokines is involved in driving cytokine expression in psoriatic tissues.
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              Psoriasis prevalence among adults in the United States.

              Psoriasis is a chronic inflammatory disorder associated with significant morbidity and mortality. Up-to-date prevalence data on psoriasis provide the foundation for informing population research, education, and health policy. We sought to determine the prevalence of psoriasis among US adults. We performed a cross-sectional study using National Health and Nutrition Examination Survey 2009 through 2010 data to determine psoriasis prevalence rates. From 6218 participants older than 20 years of age, 6216 respondents provided complete information regarding a psoriasis diagnosis. The prevalence of psoriasis among US adults ages 20 years and older is 3.2% (95% confidence interval [CI] 2.6%-3.7%). A total of 7.2 million US adults had psoriasis in 2010; an estimated 7.4 million US adults were affected in 2013. When stratifying the sample by race among those between ages 20 and 59 years, the psoriasis prevalence was highest in Caucasians at 3.6% (95% CI 2.7%-4.4%), followed by African Americans (1.9%; 95% CI 1.0%-2.8%), Hispanics (1.6%; 95% CI 0.5%-2.8%), and others (1.4%; 95% CI 0.3%-2.6%). The prevalence of psoriasis among US adults has not changed significantly since 2003 to 2004 (P > .05). Dermatologist evaluation and skin photographs were unavailable for the 2009 through 2010 surveys. In the United States, psoriasis remains a common, immune-mediated disease, affecting 7.4 million adults. Its prevalence has remained stable since the mid-2000s. Copyright © 2013 American Academy of Dermatology, Inc. Published by Mosby, Inc. All rights reserved.
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                Author and article information

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                Journal
                JCMOHK
                Journal of Clinical Medicine
                JCM
                MDPI AG
                2077-0383
                September 2022
                September 06 2022
                : 11
                : 18
                : 5254
                Article
                10.3390/jcm11185254
                29999399-fcce-4cbf-81c5-9c3a9e8b55f9
                © 2022

                https://creativecommons.org/licenses/by/4.0/

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