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Psoriasis: HELP
Articles by Charlotta Enerbäck
Based on 22 articles published since 2008
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Between 2008 and 2019, C. Enerbäck wrote the following 22 articles about Psoriasis.
 
+ Citations + Abstracts
1 Review Soluble biomarkers in psoriasis. 2011

Enerbäck, Charlotta. ·Department of Clinical and Experimental Medicine, Division of Cell Biology and Dermatology, Linköping University, SE-581 85 Linköping, Sweden. charlotta.enerback@liu.se ·Eur J Dermatol · Pubmed #21856557.

ABSTRACT: Psoriasis is a common, chronic, recurrent skin disorder, characterized by keratinocyte proliferation, T-cell activation and angiogenesis. The results of various clinical and experimental studies indicate that psoriasis is a complex, multifactorial disease with a genetic predisposition. During the past few years, many studies related to psoriasis biomarkers have been conducted. Biomarkers can relate to diagnosis, pathogenesis, prognosis, or therapeutic response. They could provide insight into disease susceptibility and natural history. The identification of biomarkers related to co-morbidities in psoriasis, such as arthritis, cardiovascular disease and the metabolic syndrome, has attracted special interest. This review presents current knowledge of soluble biomarkers in psoriasis, including cytokines, chemokines, pro-angiogenic mediators, growth factors, antimicrobial proteins, neuropeptides and markers of oxidative stress.

2 Article The Importance of Achieving Clear or Almost Clear Skin for Patients: Results from the Nordic Countries of the Global. 2019

Rasmussen, Mads Kirchheiner / Enger, Martin / Dahlborn, Anna-Karin / Juvik, Siri / Fagerhed, Laura / Dodge, Rikke / Enerbäck, Charlotta. ·Department of Dermatology, Aarhus University Hospital, Aarhus, Denmark. ·Acta Derm Venereol · Pubmed #30250961.

ABSTRACT: Psoriasis is a stigmatizing chronic skin condition in which impairment of quality of life is associated with visibility of skin lesions, disease activity and severity. The ultimate goal of treatment is complete clearance of skin symptoms. The worldwide "Clear About Psoriasis" survey explored patients' perspectives on clear/almost clear skin and the impact of psoriasis on daily life. We report here results from the Nordic countries (n = 609). Of respondents, 44% achieved clear/almost clear skin with their current treatment, of which 71% were comfortable discussing this expectation with their physician, compared with only 46% of patients who had not achieved clear/almost clear skin. Of patients who achieved clear/almost clear skin, 85% reported treatment satisfaction vs. 39% who had not. Psoriasis profoundly affected daily life, with 88% of respondents reporting discrimination/humiliation and 61% reporting an impact on their professional life. This report highlights stigmatization among Nordic patients with psoriasis and the potential to improve physician-patient communication.

3 Article The Act1 D10N missense variant impairs CD40 signaling in human B-cells. 2019

Yu, Ning / Lambert, Sylviane / Bornstein, Joshua / Nair, Rajan P / Enerbäck, Charlotta / Elder, James T. ·Department of Dermatology, University of Michigan, Ann Arbor, MI, USA. ning_yu@vip.163.com. · Department of Dermatology, Shanghai Skin Disease Hospital, Shanghai, China. ning_yu@vip.163.com. · Department of Dermatology, University of Michigan, Ann Arbor, MI, USA. · Department of Dermatology, Linköping University, Linköping, Sweden. · Department of Dermatology, University of Michigan, Ann Arbor, MI, USA. jelder@umich.edu. · Ann Arbor Veterans Affairs Health System, Ann Arbor, MI, USA. jelder@umich.edu. ·Genes Immun · Pubmed #29302052.

ABSTRACT: The TRAF3IP2 gene resides within one of at least 63 psoriasis susceptibility loci and encodes Act1, an adapter protein involved in IL-17 receptor and CD40 signaling pathways. TRAF3IP2 is distinctive (among <10% of candidate susceptibility genes) in that a strongly disease-associated variant encodes a missense SNP predicted to be functionally relevant (SNP rs33980500 C/T encoding Act1 pD10N). As assessed by flow cytometry, Act1 protein was expressed at the highest levels in monocytes, with lower levels in T-cells and B-cells. However, monocytes, T-cells and B-cells failed to respond to IL-17A stimulation of PBMC, as measured by flow cytometric determination of NF-κB phospho-p65. As an alternative stimulus, we treated PBMCs with trimerized recombinant human CD40L and assessed p65, p38 and Erk phosphorylation in CD19

4 Article Genetic signature to provide robust risk assessment of psoriatic arthritis development in psoriasis patients. 2018

Patrick, Matthew T / Stuart, Philip E / Raja, Kalpana / Gudjonsson, Johann E / Tejasvi, Trilokraj / Yang, Jingjing / Chandran, Vinod / Das, Sayantan / Callis-Duffin, Kristina / Ellinghaus, Eva / Enerbäck, Charlotta / Esko, Tõnu / Franke, Andre / Kang, Hyun M / Krueger, Gerald G / Lim, Henry W / Rahman, Proton / Rosen, Cheryl F / Weidinger, Stephan / Weichenthal, Michael / Wen, Xiaoquan / Voorhees, John J / Abecasis, Gonçalo R / Gladman, Dafna D / Nair, Rajan P / Elder, James T / Tsoi, Lam C. ·Department of Dermatology, University of Michigan Medical School, Ann Arbor, 48109, MI, USA. · Morgridge Institute for Research, Madison, 53715, WI, USA. · Ann Arbor Veterans Affairs Hospital, Ann Arbor, 48105, MI, USA. · Department of Biostatistics, Center for Statistical Genetics, University of Michigan, Ann Arbor, 48109, MI, USA. · Department of Human Genetics, Emory University School of Medicine, Atlanta, 30322, GA, USA. · Department of Medicine, Division of Rheumatology, University of Toronto, Toronto, Ontario, M5G 2C4, Canada. · Centre for Prognosis Studies in the Rheumatic Diseases, Krembil Research Institute, University of Toronto, Toronto, Ontario, M5T 2S8, Canada. · Institute of Medical Science, University of Toronto, Toronto, Ontario, M5S 1A8, Canada. · Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, M5S 1A8, Canada. · Department of Dermatology, University of Utah, Salt Lake City, Utah, 84132, USA. · Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel, 24105, Germany. · Department of Dermatology, Linköping University, Linköping, SE-581 83, Sweden. · Estonian Genome Center, University of Tartu, Tartu, 51010, Estonia. · Broad Institute of MIT and Harvard, Cambridge, Massachusetts, 02142, USA. · Department of Dermatology, Henry Ford Hospital, Detroit, 48202, MI, USA. · Memorial University, St. John's, Newfoundland and Labrador, A1B 3X9, Canada. · Division of Dermatology, Toronto Western Hospital, University of Toronto, Toronto, M5G 2C4, Ontario, Canada. · Department of Dermatology, University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, 24105, Germany. · Department of Dermatology, University of Michigan Medical School, Ann Arbor, 48109, MI, USA. alextsoi@med.umich.edu. · Department of Biostatistics, Center for Statistical Genetics, University of Michigan, Ann Arbor, 48109, MI, USA. alextsoi@med.umich.edu. · Department of Computational Medicine & Bioinformatics, University of Michigan, Ann Arbor, 4810, MI, USA. alextsoi@med.umich.edu. ·Nat Commun · Pubmed #30301895.

ABSTRACT: Psoriatic arthritis (PsA) is a complex chronic musculoskeletal condition that occurs in ~30% of psoriasis patients. Currently, no systematic strategy is available that utilizes the differences in genetic architecture between PsA and cutaneous-only psoriasis (PsC) to assess PsA risk before symptoms appear. Here, we introduce a computational pipeline for predicting PsA among psoriasis patients using data from six cohorts with >7000 genotyped PsA and PsC patients. We identify 9 new loci for psoriasis or its subtypes and achieve 0.82 area under the receiver operator curve in distinguishing PsA vs. PsC when using 200 genetic markers. Among the top 5% of our PsA prediction we achieve >90% precision with 100% specificity and 16% recall for predicting PsA among psoriatic patients, using conditional inference forest or shrinkage discriminant analysis. Combining statistical and machine-learning techniques, we show that the underlying genetic differences between psoriasis subtypes can be used for individualized subtype risk assessment.

5 Article Decreased Systemic Levels of Endocan-1 and CXCL16 in Psoriasis Are Restored following Narrowband UVB Treatment. 2018

Sigurdardottir, Gunnthorunn / Ekman, Anna-Karin / Verma, Deepti / Enerbäck, Charlotta. · ·Dermatology · Pubmed #30176661.

ABSTRACT: BACKGROUND: In psoriasis, a common immune-mediated disease affecting 2-3% of the population worldwide, there is an increased prevalence of extracutaneous diseases including obesity, the metabolic syndrome, and cardiovascular disease. This is believed to be linked to systemic inflammation. In previous studies, we have explored various markers in plasma and serum to characterize the ongoing systemic inflammation in psoriasis patients compared to controls. We have identified several markers that were altered in psoriasis patients, but which all were unresponsive to narrowband UVB (NB-UVB) treatment. OBJECTIVE: The objective of the study was to evaluate the effect of NB-UVB treatment on markers of cardiovascular risk and systemic inflammation in psoriasis. METHODS: The levels of 17 potential biomarkers with an association with cardiovascular risk were quantitated in plasma from 37 age- and gender-matched psoriasis patients and controls at baseline and in 21 psoriasis patients after 12 weeks of NB-UVB treatment to identify a systemic treatment response. RESULTS: We identified the mediators endocan-1, CXCL16, and sVEGFR1, which were systemically decreased in psoriasis at baseline, as well as FABP3, FABP4, and sIL-1R1, which showed normal baseline levels. After 10-12 weeks of NB-UVB treatment, endocan-1 and CXCL16 were restored to normal levels, while sVEGFR1, FABP3, FABP4, and sIL-1R1 showed a significant reduction. CONCLUSION: The current study expands the number of potential biomarkers in psoriasis by including a greater number and variety of mediators, approaching the systemic inflammation from additional vantage points, including soluble immune receptors and adipocyte contribution, to provide a more complete picture of the systemic inflammatory state in psoriasis.

6 Article Genome-Wide DNA Methylation Profiling Identifies Differential Methylation in Uninvolved Psoriatic Epidermis. 2018

Verma, Deepti / Ekman, Anna-Karin / Bivik Eding, Cecilia / Enerbäck, Charlotta. ·Ingrid Asp Psoriasis Research Center, Department of Clinical and Experimental Medicine, Division of Dermatology, Linköping University, Linköping, Sweden. · Ingrid Asp Psoriasis Research Center, Department of Clinical and Experimental Medicine, Division of Dermatology, Linköping University, Linköping, Sweden. Electronic address: charlotta.enerback@liu.se. ·J Invest Dermatol · Pubmed #29247660.

ABSTRACT: Psoriasis is a chronic inflammatory skin disease with both local and systemic components. Genome-wide approaches have identified more than 60 psoriasis-susceptibility loci, but genes are estimated to explain only one-third of the heritability in psoriasis, suggesting additional, yet unidentified, sources of heritability. Epigenetic modifications have been linked to psoriasis and altered DNA methylation patterns in psoriatic versus healthy skin have been reported in whole-skin biopsies. In this study, focusing on epigenetic modifications in the psoriatic uninvolved skin, we compared the lesional and non-lesional epidermis from psoriasis patients with epidermis from healthy controls. We performed an exhaustive genome-wide DNA methylation profiling using reduced representation bisulfite sequencing, which interrogates the methylation status of approximately 3-4 million CpG sites. More than 2,000 strongly differentially methylated sites were identified and a striking overrepresentation of the Wnt and cadherin pathways among the differentially methylated sites was found. In particular, we observe a strong differential methylation in several psoriasis candidate genes. A substantial number of differentially methylated sites present in the uninvolved versus healthy epidermis suggests the presence of a pre-psoriatic state in the clinically healthy skin type. Our exploratory study represents a starting point for identifying biomarkers for psoriasis-prone skin before disease onset.

7 Article Exome-wide association study reveals novel psoriasis susceptibility locus at TNFSF15 and rare protective alleles in genes contributing to type I IFN signalling. 2017

Dand, Nick / Mucha, Sören / Tsoi, Lam C / Mahil, Satveer K / Stuart, Philip E / Arnold, Andreas / Baurecht, Hansjörg / Burden, A David / Callis Duffin, Kristina / Chandran, Vinod / Curtis, Charles J / Das, Sayantan / Ellinghaus, David / Ellinghaus, Eva / Enerback, Charlotta / Esko, Tõnu / Gladman, Dafna D / Griffiths, Christopher E M / Gudjonsson, Johann E / Hoffman, Per / Homuth, Georg / Hüffmeier, Ulrike / Krueger, Gerald G / Laudes, Matthias / Lee, Sang Hyuck / Lieb, Wolfgang / Lim, Henry W / Löhr, Sabine / Mrowietz, Ulrich / Müller-Nurayid, Martina / Nöthen, Markus / Peters, Annette / Rahman, Proton / Reis, André / Reynolds, Nick J / Rodriguez, Elke / Schmidt, Carsten O / Spain, Sarah L / Strauch, Konstantin / Tejasvi, Trilokraj / Voorhees, John J / Warren, Richard B / Weichenthal, Michael / Weidinger, Stephan / Zawistowski, Matthew / Nair, Rajan P / Capon, Francesca / Smith, Catherine H / Trembath, Richard C / Abecasis, Goncalo R / Elder, James T / Franke, Andre / Simpson, Michael A / Barker, Jonathan N. ·Division of Genetics and Molecular Medicine, Faculty of Life Sciences & Medicine, King's College London, London, UK. · Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel, Germany. · Department of Dermatology. · Department of Computational Medicine & Bioinformatics, University of Michigan Medical School, Ann Arbor, MI, USA. · Department of Biostatistics, School of Public Health, University of Michigan, Ann Arbor, MI, USA. · St John's Institute of Dermatology, Faculty of Life Sciences & Medicine, King's College London, London, UK. · Clinic and Polyclinic of Dermatology, University Medicine Greifswald, Greifswald, Germany. · Department of Dermatology, Venereology and Allergy, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany. · Institute of Infection, Inflammation and Immunity, University of Glasgow, Glasgow, UK. · Department of Dermatology, University of Utah, Salt Lake City, UT, USA. · Department of Medicine. · Department of Laboratory Medicine and Pathobiology. · Institute of Medical Science, University of Toronto, Toronto, ON, Canada. · Krembil Research Institute, University Health Network, Toronto, ON, Canada. · NIHR Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London, London, UK. · Social Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK. · Division of Cell Biology and Dermatology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden. · Estonian Biobank, Estonian Genome Center, University of Tartu, Tartu, Estonia. · Dermatology Centre, Salford Royal Hospital, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK. · Genomics Research Group, Department of Biomedicine, University of Basel, Basel, Switzerland. · Institute of Human Genetics, University of Bonn, Bonn, Germany. · Department of Functional Genomics, Interfaculty Institute for Genetics and Functional Genomics, University Medicine and Ernst-Moritz-Arndt-University Greifswald, Greifswald, Germany. · Institute of Human Genetics, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. · I. Department of Medicine. · Institute of Epidemiology and Biobank PopGen, Christian-Albrechts-University of Kiel, Kiel, Germany. · Department of Dermatology, Henry Ford Hospital, Detroit, MI, USA. · Institute of Genetic Epidemiology, Helmholtz Zentrum Munich, Neuherberg, Germany. · Memorial University of Newfoundland, St. John's, NL, Canada. · Dermatological Sciences, Institute of Cellular Medicine, Newcastle University Medical School, Newcastle upon Tyne, UK. · Department of Dermatology, Royal Victoria Infirmary, Newcastle Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK. · Institute for Community Medicine, Study of Health in Pomerania/KEF, University Medicine Greifswald, Greifswald, Germany. · Dermatology Centre, Salford Road NHS Foundation Trust, Manchester Academic Health Science Centre, The University of Manchester, Manchester, UK. · Department of Dermatology, University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany. · Ann Arbor Veterans Hospital, Ann Arbor, MI, USA. ·Hum Mol Genet · Pubmed #28973304.

ABSTRACT: Psoriasis is a common inflammatory skin disorder for which multiple genetic susceptibility loci have been identified, but few resolved to specific functional variants. In this study, we sought to identify common and rare psoriasis-associated gene-centric variation. Using exome arrays we genotyped four independent cohorts, totalling 11 861 psoriasis cases and 28 610 controls, aggregating the dataset through statistical meta-analysis. Single variant analysis detected a previously unreported risk locus at TNFSF15 (rs6478108; P = 1.50 × 10-8, OR = 1.10), and association of common protein-altering variants at 11 loci previously implicated in psoriasis susceptibility. We validate previous reports of protective low-frequency protein-altering variants within IFIH1 (encoding an innate antiviral receptor) and TYK2 (encoding a Janus kinase), in each case establishing a further series of protective rare variants (minor allele frequency < 0.01) via gene-wide aggregation testing (IFIH1: pburden = 2.53 × 10-7, OR = 0.707; TYK2: pburden = 6.17 × 10-4, OR = 0.744). Both genes play significant roles in type I interferon (IFN) production and signalling. Several of the protective rare and low-frequency variants in IFIH1 and TYK2 disrupt conserved protein domains, highlighting potential mechanisms through which their effect may be exerted.

8 Article Large scale meta-analysis characterizes genetic architecture for common psoriasis associated variants. 2017

Tsoi, Lam C / Stuart, Philip E / Tian, Chao / Gudjonsson, Johann E / Das, Sayantan / Zawistowski, Matthew / Ellinghaus, Eva / Barker, Jonathan N / Chandran, Vinod / Dand, Nick / Duffin, Kristina Callis / Enerbäck, Charlotta / Esko, Tõnu / Franke, Andre / Gladman, Dafna D / Hoffmann, Per / Kingo, Külli / Kõks, Sulev / Krueger, Gerald G / Lim, Henry W / Metspalu, Andres / Mrowietz, Ulrich / Mucha, Sören / Rahman, Proton / Reis, Andre / Tejasvi, Trilokraj / Trembath, Richard / Voorhees, John J / Weidinger, Stephan / Weichenthal, Michael / Wen, Xiaoquan / Eriksson, Nicholas / Kang, Hyun M / Hinds, David A / Nair, Rajan P / Abecasis, Gonçalo R / Elder, James T. ·Department of Dermatology, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA. · Department of Biostatistics, Center for Statistical Genetics, University of Michigan, Ann Arbor, Michigan 48109, USA. · Department of Computational Medicine &Bioinformatics, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA. · 23andMe, Inc., Mountain View, California 94041, USA. · Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel 24105, Germany. · St John's Institute of Dermatology, Division of Genetics and Molecular Medicine, Faculty of Life Sciences and Medicine, King's College London, London SE1 9RT, UK. · Department of Medicine, Division of Rheumatology, University of Toronto, Toronto, Ontario, Canada M5S 1A8. · Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Research Institute, University of Toronto, Toronto, Ontario, Canada M5T 2S8. · Department of Dermatology, University of Utah, Salt Lake City, Utah 84132, USA. · Department of Dermatology, Linköping University, Linköping SE-581 83, Sweden. · Estonian Genome Center, University of Tartu, Tartu 51010, Estonia. · Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA. · Institute of Human Genetics, University of Bonn, Bonn 53127, Germany. · Division of Medical Genetics, Department of Biomedicine, University of Basel, Basel 4031, Switzerland. · Dermatology Clinic, Tartu University Hospital, Department of Dermatology and Venereology, University of Tartu, Tartu 50417, Estonia. · Department of Pathophysiology, Centre of Translational Medicine and Centre for Translational Genomics, University of Tartu, Tartu 50411, Estonia. · Department of Reproductive Biology, Estonian University of Life Sciences, Tartu 51006, Estonia. · Department of Dermatology, Henry Ford Hospital, Detroit, Michigan 48202, USA. · Department of Dermatology, University Medical Center Schleswig-Holstein, Campus Kiel, Kiel 24105, Germany. · Memorial University, St. John's, Newfoundland, Newfoundland and Labrador, Canada A1B 3X9. · Institute of Human Genetics, FAU Erlangen-Nürnberg, Erlangen 91054, Germany. · Ann Arbor Veterans Affairs Hospital, Ann Arbor, Michigan 48105, USA. · Department of Medical and Molecular Genetics, King's College London, London WC2R 2LS, UK. ·Nat Commun · Pubmed #28537254.

ABSTRACT: Psoriasis is a complex disease of skin with a prevalence of about 2%. We conducted the largest meta-analysis of genome-wide association studies (GWAS) for psoriasis to date, including data from eight different Caucasian cohorts, with a combined effective sample size >39,000 individuals. We identified 16 additional psoriasis susceptibility loci achieving genome-wide significance, increasing the number of identified loci to 63 for European-origin individuals. Functional analysis highlighted the roles of interferon signalling and the NFκB cascade, and we showed that the psoriasis signals are enriched in regulatory elements from different T cells (CD8

9 Article Involved and Uninvolved Psoriatic Keratinocytes Display a Resistance to Apoptosis that may Contribute to Epidermal Thickness. 2017

Eding, Cecilia Bivik / Enerbäck, Charlotta. ·Ingrid Asp Psoriasis Research Center, Department of Clinical and Experimental Medicine, Faculty of Medicine and Health Sciences, Linköping University, SE-581 85 Linköping, Sweden. ·Acta Derm Venereol · Pubmed #28350039.

ABSTRACT: Psoriasis is a common autoimmune skin disease. The aim of this study was to investigate whether the apoptotic process is disturbed in psoriatic keratinocytes. In vitro culture of keratinocytes derived from both involved and uninvolved psoriatic skin, revealed higher viability and resistance to apoptosis following exposure to ultraviolet B, compared with cells from healthy controls. The position of apoptotic dysregulation was found to be upstream of cytochrome c release in the mitochondrial apoptotic pathway. Microarray transcriptome analysis revealed that 87 genes were differentially expressed in both involved and uninvolved psoriatic keratinocytes compared with controls. Among these, a general upregulation of anti-apoptotic genes and downregulation of pro-apoptotic genes were identified. This distinct apoptosis-resistant phenotype, unrelated to the inflammatory component of the disease, implies that intrinsic abnormalities in keratinocytes may contribute to the pathogenesis of psoriasis.

10 Article Overexpression of Psoriasin (S100A7) Contributes to Dysregulated Differentiation in Psoriasis. 2017

Ekman, Anna-Karin / Vegfors, Jenny / Eding, Cecilia Bivik / Enerbäck, Charlotta. ·Ingrid Asp Psoriasis Research Center, Department of Clinical and Experimental Medicine, Linköping University, SE-581 85 Linköping, Sweden. ·Acta Derm Venereol · Pubmed #27958610.

ABSTRACT: Psoriasin, which is highly expressed in psoriasis, is encoded by a gene located within the epidermal differentiation complex. The aim of this study was to investigate the effect of endogenous psoriasin on disturbed keratinocyte differentiation in psoriasis. Immunohistochemical staining revealed a gradient of psoriasin expression in the psoriatic epidermis with highest expression in the suprabasal, differentiated layers. Induction of keratinocyte differentiation caused concurrent expression of psoriasin and the differentiation marker involucrin. The differentiation-induced psoriasin expression was found to be mediated by the protein kinase C pathway. The downregulation of psoriasin expression by small interfering RNA revealed that psoriasin mediates the expression of involucrin, desmoglein 1, transglutaminase 1 and CD24 in normal differentiation. The lentivirus-mediated overexpression of psoriasin, mimicking the psoriatic milieu, gave rise to an altered regulation of differentiation genes and an expression pattern reminiscent of that in psoriatic epidermis. These findings suggest that psoriasin contributes to the dysregulated differentiation process in the psoriasis epidermis.

11 Article Psoriasin (S100A7) promotes stress-induced angiogenesis. 2016

Vegfors, J / Ekman, A-K / Stoll, S W / Bivik Eding, C / Enerbäck, C. ·Department of Clinical and Experimental Medicine, Ingrid Asp Psoriasis Research Center, Linköping University, Linköping, Sweden. · Department of Dermatology, University of Michigan, Ann Arbor, MI, U.S.A. ·Br J Dermatol · Pubmed #27155199.

ABSTRACT: BACKGROUND: Vascular modifications occur early in the development of psoriasis, and angiogenesis is one of the key features in the pathogenesis of the disease. OBJECTIVES: To identify the role of the S100 protein psoriasin in psoriasis-associated angiogenesis. METHODS: The role of psoriasin in mediating angiogenesis was investigated by silencing psoriasin with small interfering RNA (siRNA) and measuring psoriasis-associated angiogenic factors in human epidermal keratinocytes. The secretion of psoriasin and the effect of psoriasin on general regulators of angiogenesis in keratinocytes, and on endothelial cell migration, proliferation, tube formation and production of angiogenic mediators, was evaluated. RESULTS: Reactive oxygen species (ROS) and hypoxia induced the expression of psoriasin. Downregulation of psoriasin in keratinocytes using siRNA altered the ROS-induced expression of the psoriasis-associated angiogenic factors vascular endothelial growth factor (VEGF), heparin-binding epidermal growth factor-like growth factor, matrix metalloproteinase 1 and thrombospondin 1. Overexpression of psoriasin altered several regulators of angiogenesis and led to the secretion of psoriasin. Treatment with extracellular psoriasin induced proliferation, migration and tube formation in dermal-derived endothelial cells to a similar extent as VEGF and interleukin-17, and induced the expression and release of proangiogenic mediators. These effects were suggested to be mediated by the PI3K and nuclear factor kappa B pathways. CONCLUSIONS: These findings suggest that psoriasin expression is promoted by oxidative stress in keratinocytes and amplifies the ROS-induced expression of angiogenic factors relevant to psoriasis. Moreover, extracellularly secreted psoriasin may act on dermal endothelial cells to contribute to key features angiogenesis.

12 Article Genome-wide Association Analysis of Psoriatic Arthritis and Cutaneous Psoriasis Reveals Differences in Their Genetic Architecture. 2015

Stuart, Philip E / Nair, Rajan P / Tsoi, Lam C / Tejasvi, Trilokraj / Das, Sayantan / Kang, Hyun Min / Ellinghaus, Eva / Chandran, Vinod / Callis-Duffin, Kristina / Ike, Robert / Li, Yanming / Wen, Xiaoquan / Enerbäck, Charlotta / Gudjonsson, Johann E / Kõks, Sulev / Kingo, Külli / Esko, Tõnu / Mrowietz, Ulrich / Reis, Andre / Wichmann, H Erich / Gieger, Christian / Hoffmann, Per / Nöthen, Markus M / Winkelmann, Juliane / Kunz, Manfred / Moreta, Elvia G / Mease, Philip J / Ritchlin, Christopher T / Bowcock, Anne M / Krueger, Gerald G / Lim, Henry W / Weidinger, Stephan / Weichenthal, Michael / Voorhees, John J / Rahman, Proton / Gregersen, Peter K / Franke, Andre / Gladman, Dafna D / Abecasis, Gonçalo R / Elder, James T. ·Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI 48109, USA. · Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI 48109, USA; Department of Biostatistics, Center for Statistical Genetics, University of Michigan, Ann Arbor, MI 48109, USA; Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, MI 48109, USA. · Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI 48109, USA; Ann Arbor Veterans Affairs Hospital, Ann Arbor, MI 48105, USA. · Department of Biostatistics, Center for Statistical Genetics, University of Michigan, Ann Arbor, MI 48109, USA. · Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, 24105 Kiel, Germany. · Department of Medicine, Division of Rheumatology, University of Toronto, Toronto, ON M5T 2S8, Canada; Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Research Institute, University of Toronto, Toronto, ON M5T 2S8, Canada. · Department of Dermatology, University of Utah, Salt Lake City, UT 84132, USA. · Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA. · Department of Clinical and Experimental Medicine, Division of Cell Biology and Dermatology, Linköping University, 581 83 Linköping, Sweden. · Department of Pathophysiology, Centre of Translational Medicine and Centre for Translational Genomics, University of Tartu, 50411 Tartu, Estonia; Department of Reproductive Biology, Estonian University of Life Sciences, 51014 Tartu, Estonia. · Dermatology Clinic, Tartu University Hospital, Department of Dermatology and Venereology, University of Tartu, 50417 Tartu, Estonia. · Estonian Genome Center, University of Tartu, 51010 Tartu, Estonia. · Department of Dermatology, University Medical Center Schleswig-Holstein, Campus Kiel, 24105 Kiel, Germany. · Institute of Human Genetics, University of Erlangen-Nuremberg, 91054 Erlangen, Germany. · Institute of Epidemiology I, Helmholtz Zentrum Munich, German Research Center for Environmental Health, 85764 Neuherberg, Germany; Institute of Medical Informatics, Biometry and Epidemiology, Ludwig-Maximilians-University, 81377 Munich, Germany; Institute of Medical Statistics and Epidemiology, Technical University Munich, 80333 Munich, Germany. · Research Unit of Molecular Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764 Neuherberg, Germany; Institute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764 Neuherberg, Germany. · Institute of Human Genetics, University of Bonn, 53127 Bonn, Germany; Department of Genomics, Life & Brain Center, University of Bonn, 53127 Bonn, Germany. · Neurologische Klinik and Poliklinik, Klinikum rechts der Isar, Technische Universität München, 80333 Munich, Germany; Institute of Neurogenomics, Helmholtz Zentrum Munchen, German Research Center for Environmental Health, 85764 Neuherberg, Germany. · Department of Dermatology, Venereology and Allergology, University of Leipzig, 04103 Leipzig, Germany. · Saint Paul Rheumatology, Eagan, MN 55121, USA. · Seattle Rheumatology Associates, 601 Broadway, Suite 600, Seattle, WA 98122, USA. · Allergy, Immunology, and Rheumatology Division, University of Rochester Medical Center, Rochester, NY 14623, USA. · National Heart and Lung Institute, Imperial College, London SW7 2AZ, UK. · Department of Dermatology, Henry Ford Hospital, Detroit, MI 48202, USA. · Memorial University, St. John's, NL A1C 5B8, Canada. · The Feinstein Institute for Medical Research, North Shore-Long Island Jewish Health System, Manhasset, NY 11030, USA. · Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI 48109, USA; Ann Arbor Veterans Affairs Hospital, Ann Arbor, MI 48105, USA. Electronic address: jelder@umich.edu. ·Am J Hum Genet · Pubmed #26626624.

ABSTRACT: Psoriasis vulgaris (PsV) is a common inflammatory and hyperproliferative skin disease. Up to 30% of people with PsV eventually develop psoriatic arthritis (PsA), an inflammatory musculoskeletal condition. To discern differences in genetic risk factors for PsA and cutaneous-only psoriasis (PsC), we carried out a genome-wide association study (GWAS) of 1,430 PsA case subjects and 1,417 unaffected control subjects. Meta-analysis of this study with three other GWASs and two targeted genotyping studies, encompassing a total of 9,293 PsV case subjects, 3,061 PsA case subjects, 3,110 PsC case subjects, and 13,670 unaffected control subjects of European descent, detected 10 regions associated with PsA and 11 with PsC at genome-wide (GW) significance. Several of these association signals (IFNLR1, IFIH1, NFKBIA for PsA; TNFRSF9, LCE3C/B, TRAF3IP2, IL23A, NFKBIA for PsC) have not previously achieved GW significance. After replication, we also identified a PsV-associated SNP near CDKAL1 (rs4712528, odds ratio [OR] = 1.16, p = 8.4 × 10(-11)). Among identified psoriasis risk variants, three were more strongly associated with PsC than PsA (rs12189871 near HLA-C, p = 5.0 × 10(-19); rs4908742 near TNFRSF9, p = 0.00020; rs10888503 near LCE3A, p = 0.0014), and two were more strongly associated with PsA than PsC (rs12044149 near IL23R, p = 0.00018; rs9321623 near TNFAIP3, p = 0.00022). The PsA-specific variants were independent of previously identified psoriasis variants near IL23R and TNFAIP3. We also found multiple independent susceptibility variants in the IL12B, NOS2, and IFIH1 regions. These results provide insights into the pathogenetic similarities and differences between PsC and PsA.

13 Article Enhanced meta-analysis and replication studies identify five new psoriasis susceptibility loci. 2015

Tsoi, Lam C / Spain, Sarah L / Ellinghaus, Eva / Stuart, Philip E / Capon, Francesca / Knight, Jo / Tejasvi, Trilokraj / Kang, Hyun M / Allen, Michael H / Lambert, Sylviane / Stoll, Stefan W / Weidinger, Stephan / Gudjonsson, Johann E / Koks, Sulev / Kingo, Külli / Esko, Tonu / Das, Sayantan / Metspalu, Andres / Weichenthal, Michael / Enerback, Charlotta / Krueger, Gerald G / Voorhees, John J / Chandran, Vinod / Rosen, Cheryl F / Rahman, Proton / Gladman, Dafna D / Reis, Andre / Nair, Rajan P / Franke, Andre / Barker, Jonathan N W N / Abecasis, Goncalo R / Trembath, Richard C / Elder, James T. ·Department of Biostatistics, Center for Statistical Genetics, University of Michigan, Ann Arbor, Michigan 48109, USA. · Division of Genetics and Molecular Medicine, King's College London, London WC2R 2LS, UK. · Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK. · Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, 24105 Kiel, Germany. · Department of Dermatology, University of Michigan, Ann Arbor, Michigan 48109, USA. · Neuroscience Research, Centre for Addiction and Mental Health, Toronto, Ontario, Canada M5T 1R8. · National Institute for Health Research (NIHR), Biomedical Research Centre, Guy's and St Thomas' NHS Foundation Trust, London SE1 9RT, UK. · Department of Dermatology, University Hospital, Schleswig-Holstein, Christian-Albrechts-University, 24105 Kiel, Germany. · Department of Pathophysiology, Centre of Translational Medicine and Centre for Translational Genomics, University of Tartu, 50409 Tartu, Estonia. · Department of Dermatology and Venereology, University of Tartu, 50409 Tartu, Estonia. · Estonian Genome Center, University of Tartu, 51010 Tartu, Estonia. · Department of Dermatology, Linköping University, SE-581 83 Linköping, Sweden. · Department of Dermatology, University of Utah, Salt Lake City, Utah 84132, USA. · Department of Medicine, Division of Rheumatology, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada M5T 2S8. · Department of Medicine, Division of Dermatology, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada M5T 2S8. · Department of Medicine, Memorial University, St John's, Newfoundland, Canada A1C 5B8. · Institute of Human Genetics, University of Erlangen-Nuremberg, Erlangen 91054, Germany. · Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AD, UK. · Ann Arbor Veterans Affairs Hospital, Ann Arbor, Michigan 48105, USA. ·Nat Commun · Pubmed #25939698.

ABSTRACT: Psoriasis is a chronic autoimmune disease with complex genetic architecture. Previous genome-wide association studies (GWAS) and a recent meta-analysis using Immunochip data have uncovered 36 susceptibility loci. Here, we extend our previous meta-analysis of European ancestry by refined genotype calling and imputation and by the addition of 5,033 cases and 5,707 controls. The combined analysis, consisting of over 15,000 cases and 27,000 controls, identifies five new psoriasis susceptibility loci at genome-wide significance (P<5 × 10(-8)). The newly identified signals include two that reside in intergenic regions (1q31.1 and 5p13.1) and three residing near PLCL2 (3p24.3), NFKBIZ (3q12.3) and CAMK2G (10q22.2). We further demonstrate that NFKBIZ is a TRAF3IP2-dependent target of IL-17 signalling in human skin keratinocytes, thereby functionally linking two strong candidate genes. These results further integrate the genetics and immunology of psoriasis, suggesting new avenues for functional analysis and improved therapies.

14 Article Genetic variations of NLRP1: susceptibility in psoriasis. 2014

Ekman, A-K / Verma, D / Fredrikson, M / Bivik, C / Enerbäck, C. ·Ingrid Asp Psoriasis Research Center, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, SE-581 85, Linköping, Sweden. ·Br J Dermatol · Pubmed #24909542.

ABSTRACT: BACKGROUND: NACHT, LRR and PYD domain-containing protein (NLRP)1 is part of the inflammasome multiprotein complex involved in the production of interleukin (IL)-1β and IL-18, two cytokines strongly implicated in psoriasis pathogenesis. Genetic variations in NLRP1 are associated with a predisposition for chronic inflammatory conditions. OBJECTIVES: The aim of the study was to investigate the role of genetic variation in the NLRP1 inflammasome in psoriasis susceptibility. MATERIAL AND METHODS: Four haplotype-tagging single-nucleotide polymorphisms (SNPs) (rs6502867, rs8079034, rs878329 and rs12150220) were investigated by TaqMan allelic discrimination in a patient sample comprising 1847 individuals from 478 families and 802 healthy controls. RESULTS: Using the transmission disequilibrium test, a significant increase in the transmission of the NLRP1 rs8079034C and rs878329C alleles to patients with psoriasis was demonstrated (P = 0·006 and P = 0·033, respectively). Furthermore, homozygosity for the rs878329C allele correlated with a younger age of onset. We also observed an increase in the expression of NLRP1 mRNA in the peripheral blood cells of patients with psoriasis. This was accompanied by a higher level of circulating IL-18 and appeared to be associated with the rs878329C allele. CONCLUSIONS: Our data support the involvement of NLRP1 and the NLRP1 inflammasome in psoriasis susceptibility and further support the role of innate immunity in psoriasis.

15 Article Systemic treatment and narrowband ultraviolet B differentially affect cardiovascular risk markers in psoriasis. 2014

Sigurdardottir, Gunnthorunn / Ekman, Anna-Karin / Ståhle, Mona / Bivik, Cecilia / Enerbäck, Charlotta. ·Ingrid Asp Psoriasis Research Center, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden. · Unit of Dermatology and Venereology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden. · Ingrid Asp Psoriasis Research Center, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden. Electronic address: charlotta.enerback@liu.se. ·J Am Acad Dermatol · Pubmed #24656729.

ABSTRACT: BACKGROUND: Psoriasis is associated with a systemic inflammation and an increased frequency of the metabolic syndrome, both of which are believed to link psoriasis to an increased risk of cardiovascular disease. OBJECTIVE: The study aimed to investigate the systemic expression of markers of cardiovascular risk and determine their response to ultraviolet B therapy and treatment with the tumor necrosis factor-alfa inhibitor, etanercept. METHODS: Six markers of cardiovascular risk were measured in 28 patients with psoriasis and 28 control subjects. RESULTS: Five of the 6 investigated markers were elevated in patients with psoriasis. Four of these correlated to the body mass index and waist-hip ratio, suggesting a link to the metabolic syndrome. Total plasminogen activator inhibitor-1 remained elevated independently of these factors. The levels of the investigated risk markers decreased considerably after tumor necrosis factor-alfa inhibitor treatment but remained unaffected by ultraviolet therapy. LIMITATIONS: A relatively limited study population and nonrandomization are limitations. CONCLUSION: These findings suggest that the choice of treatment in psoriasis may influence the cardiovascular risk in patients with psoriasis and the metabolic syndrome.

16 Article Genetic variants of the IL22 promoter associate to onset of psoriasis before puberty and increased IL-22 production in T cells. 2014

Nikamo, Pernilla / Cheuk, Stanley / Lysell, Josefin / Enerbäck, Charlotta / Bergh, Kerstin / Xu Landén, Ning / Eidsmo, Liv / Ståhle, Mona. ·Dermatology and Venereology Unit, Department of Medicine, Karolinska lnstitutet, Karolinska University Hospital, Stockholm, Sweden. · Ingrid Asp Psoriasis Research Center, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden. · Dermatology and Venereology Unit, Department of Medicine, Karolinska lnstitutet, Karolinska University Hospital, Stockholm, Sweden. Electronic address: mona.stahle@ki.se. ·J Invest Dermatol · Pubmed #24390134.

ABSTRACT: Most psoriasis susceptibility genes were identified in cohorts of mixed clinical phenotypes and the exploration of genes in clinical subtypes is scarce. IL-22 has an established role in host defense and in psoriasis skin pathology, reflecting the delicate balance between control of infection and immunopathology. In a case-control study, we compared the genetic association to IL22 in psoriasis onset in patients between 0-9 (n=207), 10-20 (n=394), and 21-40 (n=468) years with healthy controls (n=1,529). Logistic regression analysis revealed association to regulatory elements in the IL22 promoter confined to onset of psoriasis before puberty (odds ratio=1.45, P<0.0007). The associated variants contain putative binding sites for AhR, a potent inducer of IL-22 expression. In a luciferase assay, transcriptional activity of a high-risk gene variant resulted in 80% higher promoter activity (P=0.012) compared with a low-risk variant. Ex vivo stimulated T cells from peripheral blood were analyzed with flow cytometry. Children with psoriasis carrying a high-risk variant produced 1.7 times more IL-22 compared with low-risk variants (P=0.042). Our combined genetic and functional data support the notion that a genetic IL22 variant that promotes epithelial barrier defense is preferentially enriched in and may precipitate the onset of psoriasis at an early age.

17 Article Systemically elevated Th1-, Th2- and Th17-associated chemokines in psoriasis vulgaris before and after ultraviolet B treatment. 2013

Ekman, Anna-Karin / Sigurdardottir, Gunnthorunn / Carlström, Maria / Kartul, Natalja / Jenmalm, Maria C / Enerbäck, Charlotta. ·Ingrid Asp Psoriasis Research Center, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden. ·Acta Derm Venereol · Pubmed #23571825.

ABSTRACT: Chemokines may contribute to the systemic inflammation that is linked to the increased risk of co-morbidities in patients with psoriasis. The aim of this study was to investigate circulating chemokines in patients with psoriasis and their relationship to disease severity. Analysis of plasma levels of chemokines in patients with psoriasis before narrowband ultraviolet B (UVB) therapy revealed increased expression of Th1-associated CXCL9 and -10, Th2-associated CCL17 and CCL22, and Th17-associated CCL20. CCL20 correlated with disease severity. UVB therapy reduced skin symptoms, but did not affect the chemokine levels in plasma. Anti-CD3 and anti-CD28-mediated activation of peripheral blood mononuclear cells (PBMCs) caused a higher secretion of Th2 cytokine interleukin (IL)-13 by PBMCs from patients with psoriasis than from healthy controls. The sustained high expression of inflammatory chemokines is a potential link to systemic inflammation in psoriasis. UVB therapy may be a more effective treatment of local rather than systemic inflammation.

18 Article Genetic support for the role of the NLRP3 inflammasome in psoriasis susceptibility. 2012

Carlström, Maria / Ekman, Anna-Karin / Petersson, Stina / Söderkvist, Peter / Enerbäck, Charlotta. ·Division of Cell Biology and Dermatology, Department of Clinical and Experimental Medicine, Ingrid Asp Psoriasis Research Center, Faculty of Health Sciences, Linköping University, Linköping, Sweden. ·Exp Dermatol · Pubmed #23171454.

ABSTRACT: NACHT leucine-rich repeat- and PYD-containing (NLRP)3 protein controls the inflammasome by regulating caspase-1 activity and interleukin (IL)-1β processing. The contribution of IL-1β in the pathogenesis of psoriasis is well recognized. Polymorphisms in NLRP3 and caspase recruitment domain-containing protein (CARD)8, a negative regulator of caspase-1 activity, have been associated with susceptibility to common inflammatory diseases, such as Crohn's disease and rheumatoid arthritis. To investigate the role for genetic variants in the NLRP3 inflammasome in psoriasis susceptibility. In a patient sample comprising 1988 individuals from 491 families and 1002 healthy controls, genotypes for four selected single-nucleotide polymorphisms (SNPs) in NLRP3 (three SNPs) and CARD8 (one SNP) were determined by TaqMan(®) Allelic Discrimination. Using the transmission disequilibrium test (TDT), a significant increase in the transmission of the NLRP3 rs10733113G genotype to a subgroup of patients with more widespread psoriasis was demonstrated (P = 0.015). Using logistic regression analysis in 741 patients with psoriasis and 1002 controls, the CARD8 rs2043211 genotype was significantly different in cases and controls in overall terms [OR 1.3 (1.1-1.5), P = 0.004] and for both genders. Our data support the hypothesis that the inflammasome plays a role in psoriasis susceptibility.

19 Article Elevation of serum epidermal growth factor and interleukin 1 receptor antagonist in active psoriasis vulgaris. 2010

Anderson, K S / Petersson, S / Wong, J / Shubbar, E / Lokko, N N / Carlström, M / Enerbäck, C. ·Cancer Vaccine Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA. ·Br J Dermatol · Pubmed #20716221.

ABSTRACT: BACKGROUND: Psoriatic plaques present a complex expression profile, including high levels of cytokines, chemokines and growth factors. Circulating cytokines have been suggested to reflect the activation status of the inflammatory process. OBJECTIVES: To analyse 20 cytokines, chemokines and growth factors in 14 patients with psoriasis vulgaris at the start and during the course of ultraviolet B treatment. METHODS: A multiplex cytokine assay was used. RESULTS: We identified increased serum levels of epidermal growth factor (EGF) (mean 323 vs. 36·6 pg mL⁻¹, P = 0·0001), interleukin (IL)-1 receptor antagonist (mean 39·1 vs. 14·6 pg mL⁻¹, P = 0·02) and tumour necrosis factor-α (mean 7·5 vs. 4·5 pg mL⁻¹, P = 0·04) at baseline in patients with psoriasis compared with matched controls. None of these cytokines was correlated to the severity of the disease (Psoriasis Area and Severity Index) or decreased with phototherapy, suggesting that sources other than lesional skin contribute to the production of these cytokines. Using cluster analysis, we observed coordinate upregulation of EGF, IL-6, macrophage inflammatory protein-1ß and vascular endothelial growth factor. CONCLUSIONS: The sustained high expression of inflammatory circulating cytokines is a potential mechanism linking psoriasis with its extracutaneous comorbidities.

20 Article Detection of psoriasin/S100A7 in the sera of patients with psoriasis. 2009

Anderson, K S / Wong, J / Polyak, K / Aronzon, D / Enerbäck, C. ·Cancer Vaccine Center, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA. kanderson@partners.org ·Br J Dermatol · Pubmed #19016707.

ABSTRACT: BACKGROUND: Psoriasis is a disease of dysregulated inflammation and epithelial hyperproliferation in the skin, involving both the innate and adaptive immune system. Psoriatic keratinocytes express high levels of psoriasin (S100A7), a small calcium-binding protein. OBJECTIVES: To determine if patients with active psoriasis have elevated serum levels of psoriasin and psoriasin-specific autoantibodies. METHODS: Blood was collected from 14 patients with psoriasis vulgaris at the start of narrowband ultraviolet (UV) B therapy and from 11 of these patients every 2 weeks during the course of the UVB treatment. Patient and control sera were tested for psoriasin antigen levels by sandwich enzyme-linked immunosorbent assay, and for psoriasin autoantibody titres using recombinant purified psoriasin and overlapping peptides. RESULTS: We confirmed strong and specific expression of psoriasin in psoriatic epidermis by immunohistochemistry. Systemic psoriasin antigen levels tended to be lower in patients (mean 213 ng mL(-1)) than in controls (mean 331 ng mL(-1), P = 0.308) and decreased with increasing disease severity. Psoriasin-specific autoantibodies were detected in a subset of patients with psoriasis and healthy normal donors (mean 0.347 vs. 0.255 units, P = 0.246). The epitopes recognized by the autoantibodies were mapped to an external loop domain of the molecule but did not show corresponding T-cell immunogenicity. CONCLUSIONS: Although psoriasin is overexpressed in psoriatic skin lesions, systemic levels of psoriasin tended to be lower with increasing disease severity, which may be due to the presence of psoriasin-specific autoantibodies. Neither psoriasin nor psoriasin-specific autoantibodies appear to be promising serum biomarkers for clinical psoriasis.

21 Minor Lack of preclinical support for the efficacy of histone deacetylase inhibitors in the treatment of psoriasis. 2016

Ekman, A K / Enerbäck, C. ·Department of Clinical and Experimental Medicine, Ingrid Asp Psoriasis Research Center, Faculty of Health Sciences, Linköping University, Linköping, Sweden. ·Br J Dermatol · Pubmed #26153825.

ABSTRACT: -- No abstract --

22 Minor Lack of evidence for association of VEGF polymorphisms in Swedish patients with psoriasis. 2012

Carlström, Maria / Ekman, Anna-Karin / Petersson, Stina / Enerbäck, Charlotta. · ·J Invest Dermatol · Pubmed #22318385.

ABSTRACT: -- No abstract --