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      Serum TSLP is a potential biomarker of psoriasis vulgaris activity

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          Abstract

          Background

          The proallergic cytokine, thymic stromal lymphopoietin (TSLP) may synergize with T cell–derived CD40 ligand (CD40L) to allow IL-23 production in patients with psoriasis. IL-23 is a central cytokine that mediates the inappropriate immune reaction in patients with psoriasis.

          Objective

          The aim of the study was to correlate serum level of TSLP with psoriasis severity.

          Methods

          The study was carried out on 53 patients with psoriasis. They were divided into mild, moderate, and severe according to PASI score. The patients’ ages ranged from 10 to 62 years. The patients included 29 males and 24 females. A total of 53 healthy subjects with matched age and sex served as control group. Blood samples were collected from the venous blood of the patients and control subjects then the serum was separated. The serum samples were immediately frozen at -20°C. Serum TSLP was measured by Sandwich Enzyme–linked Immunosorbant Assay (ELISA).

          Results

          There was a statistically very highly significant increase ( p<0.001) in serum TSLP levels among the case group (1042.7±812.93) compared to the control group (314.21±220.78). There was also a statistically very highly significant increase ( p<0.001) in serum TSLP levels with increased psoriasis severity estimated by PASI score.

          Conclusion

          In this study, we found that serum TSLP is elevated in psoriasis patients and is correlated with disease severity.

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          A critical function for transforming growth factor-beta, interleukin 23 and proinflammatory cytokines in driving and modulating human T(H)-17 responses.

          Elisabetta Volpe, Nicolas Servant, Raphaël Zollinger … (2008)
          Interleukin 17 (IL-17)-producing T helper 17 cells (T(H)-17 cells) have been described as a T helper cell subset distinct from T helper type 1 (T(H)1) and T(H)2 cells, with specific functions in antimicrobial defense and autoimmunity. The factors driving human T(H)-17 differentiation remain controversial. Using a systematic approach combining experimental and computational methods, we show here that transforming growth factor-beta, interleukin 23 (IL-23) and proinflammatory cytokines (IL-1beta and IL-6) were all essential for human T(H)-17 differentiation. However, individual T(H)-17 cell-derived cytokines, such as IL-17, IL-21, IL-22 and IL-6, as well as the global T(H)-17 cytokine profile, were differentially modulated by T(H)-17-promoting cytokines. Transforming growth factor-beta was critical, and its absence induced a shift from a T(H)-17 profile to a T(H)1-like profile. Our results shed new light on the regulation of human T(H)-17 differentiation and provide a framework for the global analysis of T helper responses.
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            A large-scale genetic association study confirms IL12B and leads to the identification of IL23R as psoriasis-risk genes.

            Michele Cargill, Steven Schrodi, Monica Chang … (2007)
            We performed a multitiered, case-control association study of psoriasis in three independent sample sets of white North American individuals (1,446 cases and 1,432 controls) with 25,215 genecentric single-nucleotide polymorphisms (SNPs) and found a highly significant association with an IL12B 3'-untranslated-region SNP (rs3212227), confirming the results of a small Japanese study. This SNP was significant in all three sample sets (odds ratio [OR](common) 0.64, combined P [Pcomb]=7.85x10(-10)). A Monte Carlo simulation to address multiple testing suggests that this association is not a type I error. The coding regions of IL12B were resequenced in 96 individuals with psoriasis, and 30 additional IL12B-region SNPs were genotyped. Haplotypes were estimated, and genotype-conditioned analyses identified a second risk allele (rs6887695) located approximately 60 kb upstream of the IL12B coding region that exhibited association with psoriasis after adjustment for rs3212227. Together, these two SNPs mark a common IL12B risk haplotype (OR(common) 1.40, Pcomb=8.11x10(-9)) and a less frequent protective haplotype (OR(common) 0.58, Pcomb=5.65x10(-12)), which were statistically significant in all three studies. Since IL12B encodes the common IL-12p40 subunit of IL-12 and IL-23, we individually genotyped 17 SNPs in the genes encoding the other chains of these cytokines (IL12A and IL23A) and their receptors (IL12RB1, IL12RB2, and IL23R). Haplotype analyses identified two IL23R missense SNPs that together mark a common psoriasis-associated haplotype in all three studies (OR(common) 1.44, Pcomb=3.13x10(-6)). Individuals homozygous for both the IL12B and the IL23R predisposing haplotypes have an increased risk of disease (OR(common) 1.66, Pcomb=1.33x10(-8)). These data, and the previous observation that administration of an antibody specific for the IL-12p40 subunit to patients with psoriasis is highly efficacious, suggest that these genes play a fundamental role in psoriasis pathogenesis.
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              TSLP regulates intestinal immunity and inflammation in mouse models of helminth infection and colitis

              Betsy C. Taylor, Colby Zaph, Amy E. Troy … (2009)
              Intestinal epithelial cells (IECs) produce thymic stromal lymphopoietin (TSLP); however, the in vivo influence of TSLP–TSLP receptor (TSLPR) interactions on immunity and inflammation in the intestine remains unclear. We show that TSLP–TSLPR interactions are critical for immunity to the intestinal pathogen Trichuris. Monoclonal antibody–mediated neutralization of TSLP or deletion of the TSLPR in normally resistant mice resulted in defective expression of Th2 cytokines and persistent infection. Susceptibility was accompanied by elevated expression of interleukin (IL) 12/23p40, interferon (IFN) γ, and IL-17A, and development of severe intestinal inflammation. Critically, neutralization of IFN-γ in Trichuris-infected TSLPR−/− mice restored Th2 cytokine responses and resulted in worm expulsion, providing the first demonstration of TSLPR-independent pathways for Th2 cytokine production. Additionally, TSLPR−/− mice displayed elevated production of IL-12/23p40 and IFN-γ, and developed heightened intestinal inflammation upon exposure to dextran sodium sulfate, demonstrating a previously unrecognized immunoregulatory role for TSLP in a mouse model of inflammatory bowel disease.
              Article 0 comments Cited 107 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Psoriasis (Auckl)
                Journal ID (iso-abbrev): Psoriasis (Auckl)
                Journal ID (publisher-id): PTT
                Journal ID (pmc): psoriasis
                Title: Psoriasis: Targets and Therapy
                Publisher: Dove
                ISSN (Electronic): 2230-326X
                Publication date (Electronic): 30 July 2019
                Publication date Collection: 2019
                Volume: 9
                Pages: 59-63
                Affiliations
                [1 ]Department of Dermatology, Zagazig University , Zagazig, Egypt
                [2 ]Dermatology, Zagazig General Hospital , Zagazig, Egypt
                [3 ]Clinical Pathology, Zagazig University , Zagazig, Egypt
                Author notes
                Correspondence: Mohamed Ibrahim El-GhareebDepartment of Dermatology, Faculty of Medicine, Zagazig University , Zagazig44511, EgyptTel +20 109 290 7455 Email moh_elghareeb@ 123456yahoo.com
                Author information
                http://orcid.org/0000-0003-0878-7015
                Article
                Publisher ID: 212774
                DOI: 10.2147/PTT.S212774
                PMC ID: 6679690
                PubMed ID: 31440462
                SO-VID: b1d72e1e-5915-408d-9533-28d2eae66a56
                Copyright © © 2019 El-Ghareeb et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 18 April 2019
                Date accepted : 20 June 2019
                Page count
                Figures: 2, Tables: 3, References: 14, Pages: 5
                Categories
                Subject: Original Research

                Keywords: tslp,psoriasis vulgaris,serum biomarker
                Data availability:
                Keywords: tslp, psoriasis vulgaris, serum biomarker

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