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      Evaluation of serum concentrations of the selected cytokines in patients with localized scleroderma

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          Abstract

          Introduction

          Localized scleroderma is an autoimmune disease primarily affecting the skin. The cause of disease remains unexplained although environmental factors are implicated, which are likely to be responsible for activation of the endothelium and subsequent inflammation leading to excessive synthesis of collagen and extracellular matrix components.

          Aim

          To determine concentrations of interleukin (IL)-27, transforming growth factor (TGF)-β1, TGF-β2, IL-6, and sIL-6R in patients with localized scleroderma compared to controls and to assess the relations between their levels and laboratory markers.

          Material and methods

          The study encompassed 17 females with localized scleroderma (aged 25–67). The control group consisted of 30 age-matched healthy women. The blood was sampled from the basilic vein. Serum levels of cytokines were determined using ELISA.

          Results

          The TGF-β2 levels were found to be significantly lower in patients with localized scleroderma compared to controls. Concentrations of TGF-β1 were decreased in scleroderma patients when compared to controls but without statistical significance. There were no significant differences in serum IL-6, sIL-6R and IL-27 levels between patients and the control group; however, we found a significant positive correlation between the level of sIL-6 and ESR among subjects with localized scleroderma.

          Conclusions

          The findings of decreased serum levels of TGF-β1 and TGF-β2 in patients with localized scleroderma demonstrate a possible association of these cytokines with pathogenesis of the disease. The results suggest also that sIL-6R is likely to be involved in inflammation in patients with localized scleroderma.

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          Most cited references33

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          IL-27, a heterodimeric cytokine composed of EBI3 and p28 protein, induces proliferation of naive CD4+ T cells.

          An efficient Th1-driven adaptive immune response requires activation of the T cell receptor and secretion of the T cell stimulatory cytokine IL-12 by activated antigen-presenting cells. IL-12 triggers Th1 polarization of naive CD4(+) T cells and secretion of IFN-gamma. We describe a new heterodimeric cytokine termed IL-27 that consists of EBI3, an IL-12p40-related protein, and p28, a newly discovered IL-12p35-related polypeptide. IL-27 is an early product of activated antigen-presenting cells and drives rapid clonal expansion of naive but not memory CD4(+) T cells. It also strongly synergizes with IL-12 to trigger IFN-gamma production of naive CD4(+) T cells. IL-27 mediates its biologic effects through the orphan cytokine receptor WSX-1/TCCR.
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            A dominant function for interleukin 27 in generating interleukin 10-producing anti-inflammatory T cells.

            Regulatory T cells (T(reg) cells) expressing the transcription factor Foxp3 are key in maintaining the balance of immune homeostasis. However, distinct induced T regulatory type 1 (Tr1) cells that lack Foxp3 expression also regulate T cell function, mainly by producing the immunosuppressive cytokine interleukin 10 (IL-10). However, the factors required for the induction of IL-10-producing suppressive T cells are not fully understood. Here we demonstrate that dendritic cells modified by T(reg) cells induced the generation of IL-10-producing Tr1 cells. The differentiation of naive CD4+ T cells into IL-10-producing cells was mediated by IL-27 produced by the T(reg) cell-modified dendritic cells, and transforming growth factor-beta amplified the generation of induced IL-10+ Tr1 cells by IL-27. Thus, IL-27 and transforming growth factor-beta promote the generation of IL-10-producing Tr1 cells.
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              Transforming growth factor-beta in T-cell biology.

              Strict control of T-cell homeostasis is required to permit normal immune responses and prevent undesirable self-targeted responses. Transforming growth factor-beta (TGF-beta) has been shown to have an essential role in that regulation. Owing to its broad expression, and inhibitory effects on multiple cell types of the immune system, TGF-beta regulation is complex. Through advances in cell-specific targeting of TGF-beta signalling in vivo, the role of TGF-beta in T-cell regulation has become clearer. Recent in vitro studies provide a better understanding of how TGF-beta regulates T-cell homeostasis, through multiple mechanisms involving numerous cell types.
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                Author and article information

                Journal
                Postepy Dermatol Alergol
                Postepy Dermatol Alergol
                PDIA
                Advances in Dermatology and Allergology/Postȩpy Dermatologii i Alergologii
                Termedia Publishing House
                1642-395X
                2299-0046
                29 February 2016
                February 2016
                : 33
                : 1
                : 47-51
                Affiliations
                [1 ]Healthcare Center “Dermedica”, Zamosc, Poland
                [2 ]Department of Dermatology, Venereology and Pediatric Dermatology, Medical University of Lublin, Lublin, Poland
                Author notes
                Address for correspondence: Prof. Dorota Krasowska MD, PhD, Department of Dermatology, Venereology and Pediatric Dermatology, Medical University of Lublin, 13 Radziwiłłowska St, 20-080 Lublin, Poland. phone: +48 608 098 578, fax: +48 815 323 647. e-mail: dorota.krasowska@ 123456umlub.pl
                Article
                24294
                10.5114/pdia.2015.48044
                4793054
                26985179
                6b82c58a-348f-4597-8227-9a9eb1db52d3
                Copyright © 2016 Termedia

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.

                History
                : 28 February 2014
                : 17 July 2014
                Categories
                Original Paper

                localized scleroderma,morphea,cytokines,inflammation fibrosis

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