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Discover a faster, simpler path to publishing in a high-quality journal. PLOS ONE promises fair, rigorous peer review, broad scope, and wide readership — a perfect fit for your research every time. Learn Rockefeller Psoriasis Auszeichnung Submit Now. For more information about PLOS Subject Areas, click here.

Total Mendeley and CiteULike bookmarks. Sum of PLOS and PubMed Central page views and downloads. Sum of Facebook and Twitter activity. Contributed equally to this work with: Jaehwan Kim, Pranay Nadella.

Affiliation Laboratory for Investigative Dermatology, The Rockefeller University, New York, New York, United States of America.

Affiliations Laboratory for Investigative Dermatology, The Rockefeller University, New York, New York, United States of America, Harvard University, Cambridge, Massachusetts, United States of America. Affiliations Laboratory for Investigative Dermatology, The Rockefeller University, New York, New York, United States of America, School of Medicine, Stony Brook University, Stony Brook, New York, United States of America.

Affiliation The Center for Clinical and Translational Science, The Rockefeller University, New York, New York, United States of America. Affiliations The Center for Clinical and Translational Science, The Rockefeller University, New York, New York, United States of America, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America. Psoriasis, which presents as red, scaly patches on the body, is a common, autoimmune skin disease that affects 2 to 3 percent of the world population.

To leverage recent molecular findings into the personalized treatment of psoriasis, we need a strategy that integrates clinical stratification with molecular phenotyping.

In this study, we sought to stratify psoriasis patients by histological measurements of epidermal thickness, and to compare their molecular characterizations by gene expression, serum cytokines, and response to biologics. We obtained histological measures of epidermal thickness in a cohort of psoriasis patients, and identified a mixture of two subpopulations—thick and thin plaque psoriasis—from which they were derived.

This stratification was verified in a subcohort of 65 patients from a previously published study with significant differences in inflammatory cell infiltrates in the psoriatic skin. Thick and thin plaque psoriasis shared RT-PCR revealed that gene expression in thick and thin plaque psoriasis was different not only within psoriatic lesional skin but also in peripheral non-lesional skin.

Additionally, differences in circulating cytokines and their changes in response Rockefeller Psoriasis Auszeichnung biologic treatments were found between the two subgroups. All together, we were able to integrate histological stratification with molecular phenotyping as a way of exploring clinical phenotypes with different expression levels of the psoriasis transcriptome and circulating cytokines.

Kim J, Nadella P, Kim DJ, Brodmerkel C, Correa da Rosa J, Krueger JG, et al. PLoS ONE 10 7: April 21, ; Accepted: June 15, ; Published: This is an open access article distributed under the terms of the Creative Commons Attribution Licensewhich permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The authors confirm that all data underlying the findings are fully available without restriction.

All relevant data are within the paper and its Supporting Information files. The microarray and RT-PCR data are obtained from publicly accessible previous publication DOI: The authors are not aware of any affiliations, memberships, funding, or financial holdings that might be perceived as affecting the objectivity of this review. Psoriasis is a common skin disease affecting 2 to 3 percent of the world population.

It begins as red, scaly patches on the scalp, elbows, and knees that, if it progresses to severe disease, is associated with systemic inflammation and comorbidities, such as psoriatic arthritis, cardiovascular disease, diabetes, and depression [ 1 — 7 ]. Despite having a complex, multifactorial autoimmune disease etiology, our understanding of psoriasis has been rapidly expanding along with the availability of high throughput technologies for comprehensive molecular characterization [ 89 ].

Through genomic analysis, important pathogenic molecules have been identified, and a broad spectrum of anti-psoriatic agents has been developed and has been proven to be highly effective [ 10 — Rockefeller Psoriasis Auszeichnung ].

However, there is still Rockefeller Psoriasis Auszeichnung gap between the molecular findings in the laboratory and the personalized treatment of psoriasis in real-world practice.

A more complete understanding of these molecular characteristics, and the extent to which they differ between individual psoriasis patients, would provide valuable insights to their treatment.

Clinical observation alone would support the idea of a spectrum of clinical disease phenotypes that includes small and large plaque psoriasis [ 14 ], as well as notable variants like guttate and plaque forms of psoriasis. This raises the hypothesis that there are various clinical forms of psoriasis each with their own molecular profiles. Patients with thick plaques tend to associate with higher BMI and Rockefeller Psoriasis Auszeichnung arthritis, while patients with thin plaques tend to associate with guttate psoriasis and skin cancer [ 14 ].

Because measuring the epidermal thickness on an Rockefeller Psoriasis Auszeichnung of skin biopsy tissue provides the most accurate assessment of skin thickness, we investigated whether or not histological measurements of epidermal thickness can Rockefeller Psoriasis Auszeichnung used to stratify psoriasis patients into subgroups with different expression levels of the psoriasis transcriptome and different levels of circulating cytokines in response to biologic treatments.

To explore the existence of subpopulations using the measurement of epidermal thickness, we first examined the distribution of histologically measured Rockefeller Psoriasis Auszeichnung thickness of psoriasis patients from the de-identified data accumulated at our tissue bank S1 Table. As the analysis revealed two underlying distributions of epidermal thickness differences between lesional and non-lesional skin, we compared the number of inflammatory cells, expression profiles, circulating cytokines, and treatment responses to biologics between subpopulations from a subset of patients where immunohistochemical and microarray data was available [ 1516 ].

Since we analyzed data from a single study on a single platform, we could minimize batch effects that may be seen across different studies. To our knowledge, this is the first description correlating epidermal thickness, psoriasis transcriptome, circulating cytokines, and clinical responses to biologics. The tissue bank in the Laboratory for Investigative Dermatology, Rockefeller University, provided de-identified Rockefeller Psoriasis Auszeichnung thickness data of patients with moderate-to-severe psoriasis http: The data from the tissue bank had been accumulated from multiple clinical trials approved by the Rockefeller Rockefeller Psoriasis Auszeichnung Institutional Review Board.

The skin biopsy samples were collected from histologically confirmed psoriasis patients who were enrolled into an IRB-approved Phase 3, multicenter, randomized trial protocol ACCEPT trial [ 15 ]. The platform of expression profiling was Affymetrix Human Genome U Plus 2. The raw Affymetrix data CEL files were downloaded from GEO repository and expression values were obtained using GCRMA algorithm [ 17 ], while normalization einweichen bei Psoriasis samples was carried out using quantile normalization.

RT-PCR data was generated ist Nagelpsoriasis heen Applied Rockefeller Psoriasis Auszeichnung Foster City, CA Taqman gene expression assays and Taqman low-density array cards.

The microarray and RT-PCR data, and relevant Rockefeller Psoriasis Auszeichnung information were published and publicly accessible [ 16 ]. Serum cytokine data was obtained from a Rockefeller Psoriasis Auszeichnung of Rockefeller Psoriasis Auszeichnung microarray and RT-PCR studies [ 16 ], as well as from repository data of the tissue bank in the Laboratory for Investigative Dermatology, Rockefeller University.

Epidermal thickness was measured from frozen sections of psoriatic lesional and non-lesional skin biopsies. Epidermal thickness was then measured with the ImageJ program [ 18 ]. As psoriatic lesional skin should presumably be thicker than non-lesional skin of the same patient, patient data whose lesional skin was thinner than non-lesional skin was excluded for further analysis.

Inflammatory cell infiltrates were counted from frozen sections of psoriatic lesional skin biopsies. Statistical methods to analyze histologically measured epidermal thicknesses were primarily based on the hypothesis of the presence of k morphologic subpopulations. This hypothesis was translated in statistical terms to modeling epidermal thickness by a finite mixture of k Gaussian distributions, k being an unknown parameter.

The strategy can be seen as a model-based clustering approach to allocate individuals in their morphologic subpopulations and simultaneously estimate Rockefeller Psoriasis Auszeichnung parameters of their underlying Gaussian distributions.

Conditional on these findings, extensive data analysis Rockefeller Psoriasis Auszeichnung carried in a subcohort of 65 psoriasis patients to gather evidence that gene expression, pathway activity, and inflammatory cell counts differed between the two identified subpopulations.

A robust likelihood ratio statistic obtained from bootstrap Rockefeller Psoriasis Auszeichnung was used to test for the smallest number k of components compatible with the data.

The parameters of the mixture model were estimated using the Expectation Maximization EM Algorithm [ 19 ] as Rockefeller Psoriasis Auszeichnung in R package normalmixEM. Parameter estimates Rockefeller Psoriasis Auszeichnung the mixed Gaussian distributions keep the same magnitude when the EM algorithm is applied to the subcohort of Psoriasis-Behandlung Penza psoriasis patients where complete gene array profile is available.

After fitting the interaction model, comparisons of interest were assessed using linear contrasts via restricted log-likelihood maximization REMLunder the general framework of limma package. P -values from moderated paired t-test were adjusted for multiple hypotheses across genes using Benjamini-Hochberg Rockefeller Psoriasis Auszeichnung. The activity of entire signaling pathways for each sample was quantified by using a per-patient GSEA Gene Set Enrichment Analysis -like method.

GSVA is an unsupervised sample-wise enrichment method described in [ 20 ]. Enrichment scores were obtained by setting the parameter z-score in gsva function available in R package. The formulation for scores evaluation is described in [ 21 ].

The authors proposed the linear combination of normalized expression with weights in the combination being defined as for k being the number of genes in the pathway. This methodology was applied to obtain pathway enrichment scores in both microarray and RT-PCR analyses. These enrichment scores were used as inputs for the same linear mixed model framework, described previously for gene expression, in order to evaluate significant differences in thick versus thin plaques. Association between histologically measured epidermal thickness and counts for different inflammatory cells was explored through a multiple linear regression model that included epidermal thickness as the dependent variable and markers Rockefeller Psoriasis Auszeichnung inflammation as predictors.

The selection of a subset of markers significantly correlated with epidermal thickness was carried by forward stepwise selection as implemented in IBM SPSS statistics Version Partial correlation coefficients measured by beta regression coefficients were used to measure degree of association between a specific marker and the epidermal thickness.

The change in PASI was modeled using mixed effect models with time and treatment group as Psoriasis-Arthritis Medikamente effects and random intercept for each patient. Estimates for the change in treatment were obtained using least squares means and represented Rockefeller Psoriasis Auszeichnung percent of improvement.

Most of the statistical analysis was carried out in the R language version 2. IBM SPSS Statistics Version 22 was used for forward stepwise linear regression modeling. The differences in histologically measured epidermal thickness were calculated from the lesional and matched non-lesional biopsies of psoriasis Rockefeller Psoriasis Auszeichnung S1 Tableand we evaluated whether the distribution arose from multiple populations by fitting a mixture model Rockefeller Psoriasis Auszeichnung an expectation maximization algorithm see Materials and Methods [ 22 ].

Using the likelihood ratio statistic, we tested the null hypothesis of all values from the same distribution versus read article alternative hypothesis of multiple subpopulations in the distribution.

There was a significant difference in epidermal thickness of psoriatic lesions between thick and thin plaque psoriasis, Rockefeller Psoriasis Auszeichnung no difference was observed between thick and thin plaque psoriasis in Rockefeller Psoriasis Auszeichnung skin biopsies Fig 1B. A Difference in epidermal thickness between lesional and non-lesional skin. Expectation maximization algorithm identifies two underlying distributions of the epidermal thickness difference thick and thin plaque psoriasis.

B Epidermal thickness of thick and thin plaque psoriasis. C Inflammatory cell infiltrates Rockefeller Psoriasis Auszeichnung the dermis of thick and thin plaque psoriasis. Bars represent means; error bars represent standard error of the mean SEM.

We next explored the biological implications Rockefeller Psoriasis Auszeichnung the epidermal thickness-based stratification in a subcohort of 65 moderate-to-severe plaque psoriasis patients [ 16 ]. The analysis of demographic information confirmed that phenotyping of thick and thin plaque psoriasis was not associated with differences in gender, age, BMI or duration of psoriasis Table 2. Importantly, PASI or Body Surface Area BSA was not different between thick versus thin plaque psoriasis.

Although PASI assesses the induration of Rockefeller Psoriasis Auszeichnung skin, the overall score did not reflect differences in histologically measured Radiation Hormonspritzen für Psoriasis Hanf-Salbe thickness.

To verify whether or not our stratification of psoriasis patients into subgroups drew meaningful differences in psoriasis immunopathogenesis, the numbers of T cells and dendritic cells in the dermis of the skin were compared between thick and thin plaque psoriasis. Additionally, dendritic cells and T cells numbers were significantly correlated with epidermal thickness in the linear regression model correlation coefficient: To understand thick versus thin plaque psoriasis phenotypes at the genomic level, sensitivity Erholung von der Armee Psoriasis How compared the gene expression profiles of lesional and non-lesional psoriasis across the two groups, and tried to elucidate: For confirmation, we compared a meta-analysis-derived MAD3 transcriptome as a standard reference list of psoriasis transcriptomes [ 23 ] and found that The distance matrix was built based Rockefeller Psoriasis Auszeichnung Euclidean distances and Rockefeller Psoriasis Auszeichnung McQuitty algorithm was used for clustering.

B Scatter plot that displays Chili und high correlation of DEGs between thick and thin plaque psoriasis log 2 fold change.

D Differentially expressed genes among the meta-analysis derived transcriptome genes MAD3, Tian et al. To investigate different expression levels of the psoriasis transcriptome between thick and thin plaque psoriasis skin, we performed gene set variation analysis GSVA via the combined z-score method [ 21 ].

Using the established psoriasis transcriptome references [ 1623 — 28 ], psoriasis transcriptome scores in each lesional or non-lesional biopsy sample were computed from the observed gene expression levels. As shown in Fig 3the absolute values of all the psoriasis transcriptome scores in thick plaque psoriasis were consistently higher than those in thin plaque psoriasis.

It is noteworthy that the pattern is driven more by the down-regulation scores Fig 3leftrather than the up-regulation scores Fig 3right. Based on psoriasis transcriptome references, psoriasis transcriptome scores are calculated by the combined z-score gene set variation analysis GSVA method. In addition, Rockefeller Psoriasis Auszeichnung investigated if the expression levels of psoriasis genes included in the MAD3 transcriptome were different between lesional http://freierhimmel.de/naftaderm-psoriasis-bewertungen.php non-lesional skin, or if the magnitude of dysregulation was different between thick and thin plaque psoriasis.

Important genes in the MAD3 transcriptome involved in keratinocyte proliferation Kikeratinocyte adhesion cadherin 26 and desmocollin 2T H regulated cytokines IL-1B, ILA, CXCL1, CXCL2, and CXCL8T H 1-regulated cytokines CXCL11anti-inflammatory cytokine IL Rockefeller Psoriasis Auszeichnung, lipid metabolism LEP, LPL, APOBEC3A, APOBEC3A, CH25H, and APODcardiovascular disease RBP4and angiogenesis ANG were dysregulated between lesional versus non-lesional skin more strongly in thick plaque psoriasis compared to thin plaque psoriasis Table 3.

Especially ILA was noted, as recent studies have found that IL cytokines, that belong to IL-1 family, have significant role in regulation of psoriasis and psoriasis activity [ 29 — 31 Rockefeller Psoriasis Auszeichnung. Together, the data support the notion that the differences between thick versus thin plaque psoriasis phenotypes are determined by different degrees of dysregulation of the largely identical psoriasis transcriptome.

To better understand the different degrees of dysregulation of the psoriasis transcriptome between thick and thin plaque psoriasis, the expression of 70 key genes of the psoriasis transcriptome was investigated by RT-PCR in a subcohort of patients 16 thick plaque psoriasis and 20 thin plaque psoriasis. Within the Rockefeller Psoriasis Auszeichnung data, we stratified three different dysgregulation patterns of key cytokines as described in Fig 4.

A Gene expression is significantly different only within lesional skin. B Gene expression is not significantly different within both lesional and non-lesional skin. DEFB4, a T H regulated antimicrobial peptide produced by keratinocytes, followed a trend towards increased lesional versus non-lesional dysregulation in thick plaque psoriasis compared to thin plaque psoriasis 0.

The expression level of DEFB4 in thick plaque Rockefeller Psoriasis Auszeichnung was higher than the für Psoriasis Foto Kräuter level in thin plaque psoriasis within lesional skin, while no difference was seen within non-lesional skin Fig 4A.

Interestingly, the expression levels of downstream genes in IL signaling pathways, IL and LCN2, as well as IL, were higher in thick plaque psoriasis compared to thin Rockefeller Psoriasis Auszeichnung psoriasis within non-lesional skin, while there were no significant differences within lesional skin Fig 4C. Since IL levels were similar but its downstream pathway product levels were different within non-lesional skin of thick and thin plaque psoriasis, we hypothesized that systemic inflammatory differences may exist between the subtypes and further analyzed the expression of Rockefeller Psoriasis Auszeichnung cytokines and Rockefeller Psoriasis Auszeichnung inflammatory factors in blood.

We next compared changes in the cytokine levels in response to biologics. A Percent improvement in Psoriasis Area Severity Index PASI is compared between Etanercept 12 with thick plaque psoriasis and 15 with thin plaque psoriasis and Ustekinumab 90 mg treatment 12 with thick plaque psoriasis and with 12 thin plaque psoriasis.

Bars represent means; error bars represent SEM. Clinical phenotyping of thick and thin plaque psoriasis was first described in by Christensen et al. Based on clinical data collected prospectively from psoriasis patients in the Utah Psoriasis Initiative, the study described differences between thick and thin plaque psoriasis in regards to gender, BMI, psoriatic arthritis, eczema, guttate psoriasis, and skin cancer. We drew inspiration from this study, but approached phenotyping in a different way.

Instead of defining thick and thin plaque psoriasis based on the physician assessment score and patient-reported psoriasis plaque thickness at their worst, we utilized histologically measured epidermal thickness data and applied a statistical algorithm to define thick and thin plaque psoriasis.

In contrast to the previous study, our stratification does not reflect clinical prognosis over time but demonstrates a status at a single time point. However, our method assures objective stratification of thick and thin plaque psoriasis that excludes the potential bias that can arise from subjective measurement of epidermal thickness by different physicians and patients. This discrepancy in clinical observation is likely due to differences in our phenotyping approach.

We confirmed the validity of histological phenotyping thick and thin plaque psoriasis by significant differences of immunopathogenic cell numbers between groups. Then, the subgroups were compared to understand the correlation between epidermal thickness and Rockefeller Psoriasis Auszeichnung profiling.

Rather than on-and-off activation or suppression of individual genes, gene expression levels of a similar transcriptome were increased or decreased in accordance with the changes of epidermal thickness. It is noteworthy that we profiled different patterns of gene expression between thick and thin plaque psoriasis not only within psoriatic lesional skin but also in non-lesional skin by RT-PCR. Our study also supports the notion that non-lesional skin of psoriasis patients is diseased skin, as some important psoriasis genes, such as IL, IL and LCN2, were differentially expressed between thick and thin plaque psoriasis only within non-lesional skin Fig Rockefeller Psoriasis Auszeichnung. The existence of a disease phenotype in non-lesional skin of thick plaque psoriasis may represent effects of circulating cytokines to generate the phenotype.

Thick plaque psoriasis has greater amounts of mRNA in the skin and therefore more Rockefeller Psoriasis Auszeichnung are produced in psoriatic plaques. As a result, circulating inflammatory cytokines may induce downstream genes in IL signaling pathways in non-lesional skin to Rockefeller Psoriasis Auszeichnung a disease phenotype.

We compared gene expression normalized to the house-keeping gene human acidic ribosomal protein hARP. Thus, we posit that overall production of inflammatory cytokines in thick plaque lesions would be over 3 times higher in thick plaque psoriasis versus thin plaque psoriasis if the total mRNA amount were taken into account. Another limitation of this study is that multiple plaques per patient were not sampled.

As only one biopsy was taken of a typical psoriasis lesion from each psoriasis patient, lesion-to-lesion variation that might be associated with plaques at different stages of development [ Creme mit Vitamin-D-Psoriasis ] were not considered in this study.

Recent studies have explored distinct molecular subgroups within psoriasis and the heterogeneity of inflammatory and Rockefeller Psoriasis Auszeichnung networks dissecting the psoriasis transcriptome [ 38 — 40 ]. Our study added to those explorations, but took a unique approach to integrating histologically-measured clinical phenotypes with molecular phenotypes.

Rockefeller Psoriasis Auszeichnung than dissecting the psoriasis transcriptome to identify subtypes with distinct molecular signatures, we first utilized histologic measurements of epidermal thickness to subtype psoriasis, and then identified different expression levels of the common psoriasis transcriptome in skin and different levels of circulating cytokines in blood between subtypes. All together, we applied histological stratification of thick and thin plaque psoriasis to identify molecular phenotypes with different expression levels of the psoriasis transcriptome.

Different expression levels of the psoriasis transcriptome correlated with the amount of inflammatory cytokines in psoriasis skin and circulating blood. Overall, we were able to integrate histological stratification with molecular phenotyping as a way of exploring clinical phenotypes with different expression levels of psoriasis transcriptome and circulating cytokines. Conceived and designed the experiments: JK PN JCR MSF. JK PN DJK JCR MSF. JK PN DJK JCR JGK MSF. Is the Subject Area "Psoriasis" applicable to this article?

Is the Subject Area "Cytokines" applicable to this article? Is the Subject Area "Transcriptome analysis" applicable to this article?

Is the Subject Area "Gene expression" applicable to this article? Is the Subject Area "Histology" applicable to this article? Is the Subject Area "Inflammation" applicable to this article? Is the Subject Area "Skin diseases" applicable to this article? Is the Subject Area "Biopsy" applicable to this article?

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Share Sum of Facebook and Twitter Rockefeller Psoriasis Auszeichnung. Open Access Peer-reviewed Research Article. Histological Stratification of Thick and Thin Plaque Psoriasis Explores Rockefeller Psoriasis Auszeichnung Phenotypes with Clinical Implications Jaehwan KimContributed equally to this work with: Reader Comments 0 Media Coverage Figures. All Figures Next Previous. Abstract Psoriasis, which presents as red, scaly patches on the body, is a common, autoimmune Rockefeller Psoriasis Auszeichnung disease that affects 2 to 3 percent of the world population.

Michel Simon, CNRS-University of Toulouse, FRANCE Received: July 15, Copyright: This is Rockefeller Psoriasis Auszeichnung open access article distributed under the terms of the Creative Commons Attribution Licensewhich permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Data Availability: Introduction Psoriasis is a common skin disease affecting 2 to 3 percent of the world population.

Materials and Methods The experimental data The tissue bank in the Laboratory for Investigative Dermatology, Rockefeller University, provided de-identified epidermal thickness data of patients with moderate-to-severe psoriasis http: Epidermal thickness and inflammatory cell infiltrates measurement Epidermal thickness was measured from frozen sections Rockefeller Psoriasis Auszeichnung psoriatic lesional and non-lesional skin biopsies. Statistical Analysis Statistical methods to analyze histologically measured epidermal thicknesses were primarily based on the hypothesis of the presence of k morphologic subpopulations.

Histologically measured epidermal thickness of moderate-to-severe psoriasis patients. Analysis Rockefeller Psoriasis Auszeichnung Arrays, RT-PCR, Rockefeller Psoriasis Auszeichnung circulating cytokines.

Correlation Analysis of Epidermal Thickness versus Markers for inflammation. Demographic and clinical characteristics of thick and thin plaque psoriasis. Thick and thin plaque psoriasis share the psoriasis transcriptome but the expression levels are different To understand thick versus Rockefeller Psoriasis Auszeichnung plaque go here phenotypes at the genomic level, we compared the gene expression profiles of lesional and non-lesional psoriasis across the two groups, and tried to elucidate: Comparison of check this out expressed genes DEGs between thick and thin plaque psoriasis.

Rockefeller Psoriasis Auszeichnung of psoriasis transcriptome scores between thick and thin plaque psoriasis. Comparing differentially expressed genes DEGs included in the meta-analysis-derived MAD3 transcriptome between thick and thin plaque psoriasis. Gene expression of thick and thin plaque psoriasis is different not only within psoriatic lesional skin but also in peripheral non-lesional skin To better understand the different degrees Rockefeller Psoriasis Auszeichnung dysregulation of the psoriasis transcriptome between thick and thin plaque psoriasis, the expression of 70 key genes of the psoriasis transcriptome was investigated by RT-PCR in a subcohort of patients 16 thick plaque psoriasis and 20 thin plaque psoriasis.

Comparison of psoriatic gene expression normalized to the house-keeping gene, human acidic ribosomal protein hARP. Comparison of treatment response between thick and thin plaque psoriasis. Discussion Clinical phenotyping of thick and thin plaque psoriasis was first described in by Christensen et al.

Conclusions All together, we applied histological stratification of thick and thin plaque psoriasis to identify molecular phenotypes with different expression levels of the psoriasis transcriptome. Forward stepwise linear regression model to predict epidermal thickness. Histological measures of epidermal thickness in a cohort of patients. Author Contributions Conceived and designed the Rockefeller Psoriasis Auszeichnung Boehncke WH, Boehncke S, Tobin AM, Kirby B. Advances in psoriasis treatment.

Population-based epidemiologic study Rockefeller Psoriasis Auszeichnung psoriasis with emphasis on quality of life assessment. Gladman D, Antoni C, Mease P, Clegg D, Nash P. Annals of the Rheumatic Diseases. Neimann AL, Shin DB, Wang X, Margolis DJ, Troxel AB, Gelfand JM. Prevalence of cardiovascular risk factors in patients with psoriasis.

Journal of the American Academy of Dermatology. Cohen AD, Van-Dijk D, Naggan L, Vardy DA. Factor analysis of the Beer Sheva Psoriasis Severity Score BPSS.

The Israel Medical Association journal: Devrimci-Ozguven H, Kundakci TN, Kumbasar H, Boyvat A. The depression, anxiety, life satisfaction and affective expression levels in Rockefeller Psoriasis Auszeichnung patients.

Journal of the European Academy of Dermatology and Venereology: Bhalerao J, Bowcock AM. The genetics of psoriasis: Chandran V, Rockefeller Psoriasis Auszeichnung SP. Geoepidemiology and environmental factors of psoriasis and psoriatic arthritis. Krueger GG, Langley RG, Leonardi C, Yeilding N, Guzzo Rockefeller Psoriasis Auszeichnung, Wang Y, et al. New England Journal of Medicine. Schmitt J, Zhang Z, Wozel G, Meurer M, Kirch W. Efficacy and tolerability of biologic and nonbiologic systemic treatments for moderate-to-severe psoriasis: British Journal of Dermatology.

Reich K, Burden A, Eaton J, Hawkins N. Efficacy of biologics in the treatment of moderate to severe psoriasis: Therapeutic targeting of IL for psoriasis. Christensen TE, Callis KP, Papenfuss J, Hoffman MS, Hansen CB, Wong B, et al. Observations of psoriasis in the absence of therapeutic intervention identifies two unappreciated morphologic variants, thin-plaque and thick-plaque psoriasis, and their associated phenotypes. The Journal of investigative dermatology.

Griffiths CE, Strober BE, van de Kerkhof P, Ho V, Fidelus-Gort R, Yeilding N, et al. Comparison of ustekinumab and etanercept for Rockefeller Psoriasis Auszeichnung psoriasis. The New England journal of medicine. Expanding the psoriasis disease profile: Journal of Investigative Dermatology. Wu Z, Irizarry RA, Gentleman R, Martinez-Murillo F, Spencer F. A model-based background adjustment for oligonucleotide expression arrays.

Journal of the American statistical Association. ImageJ, US National Institutes of Health, Bethesda, Maryland, USA. A primary role for vasopressin in the genesis of essential hypertension. Lee E, Chuang HY, Kim JW, Ideker T, Lee D. Rockefeller Psoriasis Auszeichnung pathway activity toward precise disease classification.

McLachlan G, Peel D. Tian S, Krueger JG, Li K, Jabbari A, Brodmerkel C, Lowes MA, et al. Meta-analysis derived MAD transcriptome of psoriasis defines the "core" pathogenesis of disease. Evaluation of the Psoriasis Transcriptome across Rockefeller Psoriasis Auszeichnung Studies by Gene Set Enrichment Wo eine bessere von Psoriasis GSEA.

Gudjonsson JE, Ding J, Li X, Nair RP, Tejasvi T, Qin ZS, et al. Global gene expression analysis reveals evidence for decreased lipid biosynthesis and increased innate immunity in uninvolved psoriatic skin. Bowcock please click for source Shannon W, Du F, Duncan Psoriasis logti, Cao K, Aftergut K, et al. Insights into psoriasis and other inflammatory diseases from large-scale gene expression Rockefeller Psoriasis Auszeichnung. Transcriptional profiling of psoriasis using RNA-seq reveals previously unidentified differentially expressed genes.

Yao Y, Richman L, Morehouse C, De Los Reyes M, Higgs BW, Boutrin A, et al. Keermann M, Koks S, Reimann E, Prans E, Abram K, Kingo K. Transcriptional landscape of psoriasis identifies the involvement of IL36 and IL36RN. Johnston A, Xing X, Guzman AM, Riblett M, Loyd CM, Ward NL, et al. Garlanda C, Dinarello CA, Mantovani A. Kim J, Krueger JG. The Immunopathogenesis of Psoriasis. Arican O, Aral M, Sasmaz S, Ciragil P. Serum TNF-alpha levels correlate with disease severity and are reduced by effective therapy in plaque-type psoriasis.

Journal of biological regulators and homeostatic agents. Gottlieb A, Menter A, Mendelsohn A, Shen Y-K, Li S, Guzzo C, Rockefeller Psoriasis Auszeichnung al. Weinblatt ME, Kremer JM, Bankhurst AD, Bulpitt KJ, Fleischmann RM, Fox RI, et al. A trial of etanercept, a recombinant tumor necrosis factor receptor: Fc fusion protein, in patients with rheumatoid arthritis receiving methotrexate. Bimodal immune activation in psoriasis. Ainali C, Valeyev N, Perera G, Williams A, Gudjonsson JE, Ouzounis CA, et al.

Transcriptome classification reveals molecular subtypes in psoriasis. Swindell WR, Xing X, Stuart PE, Chen CS, Aphale A, Nair RP, et al.

Heterogeneity of inflammatory and cytokine networks in chronic plaque psoriasis. Swindell WR, Johnston A, Voorhees JJ, Elder JT, Gudjonsson JE. Dissecting the psoriasis transcriptome: Inflammatory-and cytokine-driven gene expression in lesions Rockefeller Psoriasis Auszeichnung patients. Print Print article EzReprint. We want your feedback.

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