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<rss version="2.0"><channel><title>Neue Studien: Europe PMC</title><link>https://www.psoriasis-news.de/articles.html/1_articles/page/4/?d=1</link><description>Neue Studien: Europe PMC</description><language>de</language><item><title>Plaque-Type Psoriasis Induced by Non-Steroidal Aromatase Inhibitor (Letrozole): A Case Series</title><link>https://www.psoriasis-news.de/articles.html/1_articles/plaque-type-psoriasis-induced-by-non-steroidal-aromatase-inhibitor-letrozole-a-case-series-r623/</link><description><![CDATA[<small>No abstract supplied.</small><p><a href="http://europepmc.org/article/PMC/PMC13192298?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">623</guid><pubDate>Mon, 25 May 2026 08:01:40 +0000</pubDate></item><item><title>Puerarin attenuates keratinocyte proliferation and inflammatory responses in psoriasis via downregulating TIMP2 and alleviating endoplasmic reticulum stress.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/puerarin-attenuates-keratinocyte-proliferation-and-inflammatory-responses-in-psoriasis-via-downregulating-timp2-and-alleviating-endoplasmic-reticulum-stress-r619/</link><description><![CDATA[Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation and aberrant immune responses. Puerarin (PUE), a natural isoflavone from <i>Pueraria lobata</i>, exhibits multiple pharmacological activities, but its role in psoriasis remains unclear. The M5-induced HaCaT cell model was used to evaluate the effects of PUE on proliferation, apoptosis, and inflammation. Cell viability, proliferation, and apoptosis were assessed by CCK-8, EdU, and flow cytometry, while cytokine levels were measured by ELISA. TIMP2 and endoplasmic reticulum (ER) stress-related proteins were detected by RT-qPCR and Western blot. A TIMP2 overexpression assay was performed to verify the mechanism. PUE showed no cytotoxicity in HaCaT cells, but significantly inhibited M5-induced proliferation and inflammatory cytokine release while promoting apoptosis. Mechanistically, PUE reduced the expression of TIMP2 and ERS-related proteins, and TIMP2 overexpression partially reversed these effects. PUE alleviates proliferation and inflammation of keratinocytes in association with downregulation of TIMP2 and inhibition of ER stress-related markers, suggesting that the TIMP2-ERS axis may be implicated as a potential therapeutic target in psoriasis.<h4>Supplementary information</h4>The online version contains supplementary material available at 10.1007/s10616-026-00969-x.<p><a href="http://europepmc.org/article/MED/42117030?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">619</guid><pubDate>Thu, 14 May 2026 18:05:26 +0000</pubDate></item><item><title>Psoriatic arthritis spectrum in children: a multicentre observational study.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/psoriatic-arthritis-spectrum-in-children-a-multicentre-observational-study-r618/</link><description><![CDATA[<h4>Objectives</h4>The aim of this study is to describe characteristics of children with the International League of Associations for Rheumatology (ILAR)-defined juvenile idiopathic arthritis (JPsA) and to assess whether more sensitive and specific criteria for defining JPsA can be identified.<h4>Methods</h4>A retrospective observational multicentre study was conducted including patients with a diagnosis of JPsA according to ILAR criteria. In this population, we identified clusters using as variables the clinical criteria of JPsA according to ILAR and the CASPAR clinical criteria. In addition, we defined as undifferentiated arthritis patients that met the ERA criteria, as defined by ILAR, and presented psoriatic features such as psoriasis or a history of psoriasis or psoriatic arthritis in a first-degree relative.<h4>Results</h4>73 patients were enrolled. Three clinical clusters were found using unsupervised principal component analysis for the patients. Cluster 1 differed significantly for older patients and psoriasis. In contrast, Cluster 2 was mainly characterised by dactylitis and Cluster 3 was defined by family history of psoriasis and a significant prevalence of dactylitis. We also showed a statistically significant presence of familiarity for psoriatic arthritis in Cluster 2. The significance for all parameters evaluated did not change even when we included the patients with undifferentiated arthritis, except for MTX treatment, which was significantly more common in Cluster 2 (p=0.02), and tenosynovitis, also in Cluster 2 (p=0.05). Moreover, we evaluated our cohort by the Vancouver criteria. Combining the ILAR, CASPAR, and Vancouver criteria only two patients remain undifferentiated.<h4>Conclusions</h4>Our study showed three clinical clusters with diverse demographic and clinical characteristics, indicating JPsA heterogeneity. The findings highlight the need to look beyond ILAR criteria for clinical variables, including family history of psoriatic arthritis. The ILAR, CASPAR, and Vancouver criteria improve the diagnosis of paediatric psoriatic spectrum arthritis. This complex disease population needs larger cohorts and clinical data, especially on axial involvement, to better categorisation and treatment.<p><a href="http://europepmc.org/article/MED/42099272?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">618</guid><pubDate>Thu, 14 May 2026 18:05:26 +0000</pubDate></item><item><title>Gentiopicroside Ameliorates Psoriasis-Like Dermatitis by Modulating Immune Homeostasis and Suppressing NF-&#x3BA;B Activation.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/gentiopicroside-ameliorates-psoriasis-like-dermatitis-by-modulating-immune-homeostasis-and-suppressing-nf-%CE%BAb-activation-r617/</link><description><![CDATA[Psoriasis is a common chronic immune-mediated inflammatory skin disease that presents significant challenges in clinical management. Gentiopicroside (GPS), a bioactive compound derived from Gentiana scabra, has been reported to possess anti-inflammatory and immunomodulatory properties. However, its potential role in the treatment of psoriasis remains unclear. This study aimed to investigate the therapeutic effects of GPS on psoriasis-like dermatitis and elucidate its underlying mechanisms. A psoriasis-like dermatitis model was established in BALB/c mice using imiquimod (IMQ). The therapeutic efficacy of GPS was evaluated based on clinical and histopathological improvements. Flow cytometry was used to analyze immune cell populations in the spleen and peripheral blood. In vitro, the effects of GPS on bone marrow-derived dendritic cells (BMDCs) were assessed in an inflammatory model. RNA sequencing was performed to identify differentially expressed genes and key signaling pathways in BMDCs after GPS treatment. Molecular docking was employed to predict the binding affinity between GPS and potential targets, which were further validated using Western blotting and immunofluorescence. GPS treatment significantly alleviated psoriasis-like skin lesions in IMQ-induced mice, improving both clinical manifestations and histopathological alterations. GPS reduced the proportions of lymphocytes and dendritic cells and attenuated Th17-driven inflammation, thereby contributing to a more balanced immune milieu. In vitro, GPS inhibited the maturation and activation of BMDCs. Transcriptomic profiling demonstrated that GPS modulated multiple immune- and cytokine-associated pathways, particularly the NF-κB signaling pathway. Molecular docking suggested a strong binding affinity between GPS and NF-κB p65, while Western blotting and immunofluorescence confirmed that GPS suppressed phosphorylated NF-κB p65 nuclear translocation. GPS exerts anti-psoriatic effects through multimodal mechanisms, including immunomodulation and suppression of NF-κB activation. These findings provide experimental evidence and a theoretical basis for the development of GPS as a potential therapeutic agent for psoriasis.<p><a href="http://europepmc.org/article/MED/42093619?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">617</guid><pubDate>Thu, 14 May 2026 18:05:26 +0000</pubDate></item><item><title>Sociodemographic Factors Associated With Diagnosed Psoriasis in U.S. Adults: Patterns and Trends From NHANES and NHIS, 2003-2024.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/sociodemographic-factors-associated-with-diagnosed-psoriasis-in-us-adults-patterns-and-trends-from-nhanes-and-nhis-2003-2024-r616/</link><description><![CDATA[<h4>Objective</h4>To quantify sociodemographic differences in the prevalence of diagnosed psoriasis and to evaluate temporal trends in its epidemiologic distribution.<h4>Methods</h4>Data from the 2003-2006 and 2009-2014 National Health and Nutrition Examination Survey and the 2023-2024 National Health Interview Survey were analyzed. Meta-analysis was performed to determine whether age, sex, race/ethnicity, interview language, marital status, BMI, education, income, and health insurance are independently associated with odds of diagnosed psoriasis. Estimates from each survey period were tested for linear trends over time.<h4>Results</h4>The total sample included 53,225 participants. Spanish speakers, compared to English speakers, demonstrated markedly lower prevalence of diagnosed psoriasis (pooled aOR = 0.40, 95% CI = 0.25-0.65), even after adjusting for other sociodemographic factors including race/ethnicity. Other factors independently associated with psoriasis were older age, non-Hispanic White race/ethnicity, and higher BMI (all <i>P</i> &lt; 0.001). No temporal trends in prevalence were found in any sociodemographic subgroup.<h4>Conclusion</h4>This analysis of national data covering an almost 25-year period indicates psoriasis has consistently been one of the most common inflammatory skin diseases with a stable sociodemographic distribution over this time. High rates of potentially undiagnosed psoriasis among vulnerable sociodemographic subgroups may be a persistent issue spanning over 2 decades. Patients with limited English proficiency may have difficulty interacting with the healthcare system, leading to undiagnosed psoriasis. Difficulty of diagnosis in patients with skin of color may also contribute. Given that psoriasis is a condition with systemic effects, including impacts on cardiovascular risk, accurate and timely diagnosis is essential to ensure appropriate clinical management.<p><a href="http://europepmc.org/article/MED/42083649?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">616</guid><pubDate>Thu, 14 May 2026 18:05:26 +0000</pubDate></item><item><title>Targeting serine/glycine metabolism to attenuate IFN-&#x3B3;- and IL-22-driven inflammation and hyperproliferation in psoriasis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/targeting-serineglycine-metabolism-to-attenuate-ifn-%CE%B3-and-il-22-driven-inflammation-and-hyperproliferation-in-psoriasis-r615/</link><description><![CDATA[Psoriasis is a chronic skin disease characterized by keratinocyte hyperproliferation and inflammation, largely driven by the cytokines IL-22 and interferon (IFN)-γ. These cytokines activate the signal transducer and activator of transcription (STAT) 3 and STAT1 molecular pathways, leading to abnormal proliferation, impaired differentiation, and increased production of inflammatory mediators in keratinocytes. While the IL-22/STAT3 pathway primarily promotes de-differentiation in keratinocytes, IFN-γ/STAT1-3 signaling induces pronounced inflammation, despite exerting antiproliferative effects on these cells. Recent research has highlighted the role of serine/glycine metabolism in the pathogenesis of psoriasis, by supporting T cell and keratinocyte proliferation. Furthermore, pharmacological inhibition of serine catabolism through targeting serine hydroxymethyltranferase (SHMT)1/2 enzymes reduced the infiltration of inflammatory cells in the skin of the imiquimod-induced mouse model of psoriasis. This study investigates the role of serine catabolism in psoriasis, focusing on its influence on keratinocyte proliferation and inflammation. We examined how pharmacological inhibition of SHMT1/2, mediated by a folate-competitive cell-permeable inhibitor Serine Hydroxymethyltransferase INhibitor 1 (SHIN1), affects keratinocyte proliferation and inflammatory signaling pathways in response to psoriasis-associated cytokines IL-22 and IFN-γ, using both in vitro and ex vivo models of the disease. We found that SHIN1 reduced keratinocyte proliferation, particularly under IL-22 stimulation, and restored differentiation in ex vivo psoriasis skin explants by reversing the effects of IL-22. SHIN1 also inhibited IFN-γ-induced expression of pro-inflammatory genes (e.g., CXCL10, CXCL9, CCL5, CCL2, IL-6) and reduced STAT3 activation, with only modest effects on STAT1 and extracellular signal-regulated kinase 1/2 activation. In psoriasis explants, SHIN1 decreased the expression of Ki67, Keratin 16, and pro-inflammatory cytokines including IL-17A, IL-22, and IFN-γ. These findings support the therapeutic potential of SHIN1 as a metabolism-targeted agent for psoriasis and other cytokine-mediated skin disorders, providing a rationale for further exploration of novel treatment strategies.<p><a href="http://europepmc.org/article/MED/42103703?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">615</guid><pubDate>Thu, 14 May 2026 18:05:26 +0000</pubDate></item><item><title>Immunohistochemistry Revealed Distinct IL-36&#x3B3; Localization Among Different Skin Diseases.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/immunohistochemistry-revealed-distinct-il-36%CE%B3-localization-among-different-skin-diseases-r614/</link><description><![CDATA[IL-36γ is highly expressed in psoriatic skin lesions and promotes neutrophil infiltration through the induction of neutrophil chemotactic chemokines. While IL-36γ has been established to play an important role in the pathogenesis of psoriasis, its localization in the psoriatic epidermis has not been fully elucidated, and the difference in its expression patterns among other inflammatory skin diseases remains unclear. We investigated IL-36γ localization using immunohistochemistry in skin specimens from patients with psoriasis vulgaris (n = 36), generalized pustular psoriasis (n = 11), pyoderma gangrenosum (n = 6), palmoplantar pustulosis (n = 6), tumor necrosis factor inhibitor-induced paradoxical reaction (n = 3), pustular drug eruption (n = 5), atopic dermatitis (n = 11), tinea infection (n = 3), and mycosis fungoides (n = 9), as well as uninvolved skin adjacent to benign tumors (n = 4). Staining scores were assessed based on intensity and distribution, and nuclear positivity was compared among diseases. IL-36γ was strongly expressed in the upper epidermis of psoriasis vulgaris and generalized pustular psoriasis, with staining scores significantly higher than those in atopic dermatitis and adjacent normal skin. Expression in pyoderma gangrenosum, palmoplantar pustulosis, paradoxical reaction, and pustular drug eruption was comparable to psoriasis vulgaris. Nuclear staining of IL-36γ was frequent in psoriasis vulgaris (33/36, 92%) and generalized pustular psoriasis (11/11, 100%), but absent in pyoderma gangrenosum. The difference in nuclear positivity between psoriasis and pyoderma gangrenosum was statistically significant. These findings confirm that IL-36γ is highly expressed in psoriatic lesions but is not specific to psoriasis, as it is also upregulated in other inflammatory skin diseases. Nuclear staining was observed in psoriasis but not in pyoderma gangrenosum, suggesting a potential disease-specific localization pattern. The biological significance and mechanism of nuclear localization remain unclear, as the IL-36γ molecule lacks a nuclear localization signal. Our findings highlight that the localization of IL-36γ differs among inflammatory skin diseases, suggesting that it may reflect pathogenic differences and warrant further investigation.<p><a href="http://europepmc.org/article/MED/42076875?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">614</guid><pubDate>Thu, 14 May 2026 18:05:26 +0000</pubDate></item><item><title>Promoting keratinocyte psoriasiform changes and IL-17RE expression: Potential role of GLT1D1 in linear psoriasis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/promoting-keratinocyte-psoriasiform-changes-and-il-17re-expression-potential-role-of-glt1d1-in-linear-psoriasis-r613/</link><description><![CDATA[<h4>Background</h4>Linear psoriasis is a rare variant of psoriasis characterized by erythema and scaling along the Blaschko lines. Its pathogenesis remains unknown.<h4>Objective</h4>To investigate the molecular and immunological mechanisms of linear psoriasis through gene mutation analysis and in vitro experiments and identify potential combined therapeutic targets for psoriasis.<h4>Methods</h4>Whole-exome sequencing was performed on linear lesion, clinically normal skin, and peripheral blood from linear psoriasis patient to identify somatic mutations. Candidate gene expression was assessed using public RNA-seq data of linear and classic psoriasis vulgaris, dataset before and after IL-17 antagonist Brodalumab treatment, and single-cell data of recurrent psoriasis lesions. Immunofluorescence staining confirmed gene expression and distribution. In vitro keratinocyte assays evaluated effects on proliferation and inflammation. Based on these findings, the patient received IL-17 antagonist therapy (Ixekizumab).<h4>Results</h4>An increased copy number variant of Glycosyltransferase 1 Domain Containing 1 (GLT1D1), not previously reported, was identified in the epidermis of linear psoriasis. GLT1D1 was highly expressed in both linear psoriasis and classic psoriasis vulgaris, as well as in recurrent lesions and in patients who failed to achieve PASI75 with IL-17 antagonist therapy. In keratinocytes, GLT1D1 overexpression promoted cell proliferation, enhanced proinflammatory cytokine secretion, and activated IL-17 signaling, particularly via IL-17RE upregulation. In imiquimod-induced mouse models, GLT1D1 overexpression aggravated psoriasiform inflammation. Clinical improvement was observed in the patient after treatment with ixekizumab.<h4>Conclusion</h4>GLT1D1, with an abnormally high copy number, may contribute to psoriasiform changes in keratinocytes by promoting proliferation, increasing proinflammatory cytokine secretion, and enhancing IL-17RE expression.<p><a href="http://europepmc.org/article/MED/42090972?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">613</guid><pubDate>Thu, 14 May 2026 18:05:26 +0000</pubDate></item><item><title>Impact of biologic class and treatment line on psoriatic arthritis risk in psoriasis: a population-based cohort study.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/impact-of-biologic-class-and-treatment-line-on-psoriatic-arthritis-risk-in-psoriasis-a-population-based-cohort-study-r612/</link><description><![CDATA[<h4>Background</h4>Patients with psoriasis (PsO) are at increased risk of developing psoriatic arthritis (PsA). Emerging evidence suggests that biologic therapies may differentially influence the development of PsA; however, there are no data on the relative ability of second-line biological therapy to prevent PsA.<h4>Aim</h4>To evaluate the impact of biologic therapy on the risk of incident PsA in patients with PsO with a focus on second-line biologic therapy.<h4>Methods</h4>We identified 2819 patients who initiated biologic therapy for PsO between 2002 and 2022, including Tumor Necrosis Factor (TNF) inhibitors, interleukin (IL)-17 inhibitors, IL-23p19 inhibitors and IL-12/23 inhibitors. The primary outcome was incident PsA. Kaplan-Meier survival analysis and Cox proportional hazards models were used to evaluate arthritis-free survival and HRs for the development of PsA. Risk was assessed separately for first-line and second-line biologic therapy.<h4>Results</h4>Among 2819 patients with PsO initiating first-line biologic therapy, 400 (14.2%) developed PsA. In multivariable Cox regression, first-line anti-IL-23p19 agents were significantly associated with a lower risk of developing PsA compared with TNF inhibitors (HR 0.13; 95% CI 0.02 to 0.96; p=0.045). Among 1246 patients receiving second-line biologics, 125 (10.0%) developed PsA. Notably, in second-line therapy, only IL-17 inhibitors were independently associated with a statistically significant reduction in PsA risk versus TNF inhibitors (HR 0.37; 95% CI 0.16 to 0.85; p=0.019), with trends observed for anti-IL-12/23 (HR 0.14; 95% CI 0.02 to 1.05; p=0.056) and anti-IL-23p19 (HR 0.46; 95% CI 0.20 to 1.07; p=0.070).<h4>Conclusions</h4>This is the first study to evaluate second-line biological therapy in relation to PsA risk. IL-17 inhibitor therapy was significantly associated with a reduced risk of incident PsA compared with TNF inhibitors.<p><a href="http://europepmc.org/article/MED/42097693?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">612</guid><pubDate>Thu, 14 May 2026 18:05:26 +0000</pubDate></item><item><title>Complete clearance of high-impact sites with risankizumab in patients with psoriasis: a 2-year real-world retrospective multicenter cohort study.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/complete-clearance-of-high-impact-sites-with-risankizumab-in-patients-with-psoriasis-a-2-year-real-world-retrospective-multicenter-cohort-study-r611/</link><description><![CDATA[<h4>Objectives</h4>Plaque psoriasis frequently involves high-impact anatomical sites such as the scalp, nails, and palmoplantar regions, which are associated with significant functional impairment and reduced quality of life. Evidence on the long-term effectiveness of biologic therapies in these locations in real-world settings remains limited. This study aimed to evaluate the real-world effectiveness and safety outcomes of risankizumab in achieving complete clearance of psoriasis affecting high-impact sites over a 2-year period.<h4>Methods</h4>We conducted a retrospective multicenter cohort study including adult patients with plaque psoriasis who initiated risankizumab between January 2020 and December 2023 across six dermatology centers. Effectiveness was assessed as the proportion of patients achieving complete clearance (Physician Global Assessment score of 0) in scalp, nail, and palmoplantar psoriasis.<h4>Results</h4>Among 459 patients treated with risankizumab, 232 (50.5%) had involvement of at least one high-impact site at baseline. Complete clearance at 2 years was achieved in 72.5% of patients with scalp involvement, 64.7% of those with nail psoriasis, and 52.2% of those with palmoplantar disease. Adverse events were infrequent and not treatment-limiting.<h4>Conclusions</h4>These findings support the effectiveness of risankizumab in high-impact psoriasis sites in real-world clinical practice.<p><a href="http://europepmc.org/article/MED/42089713?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">611</guid><pubDate>Thu, 14 May 2026 18:05:26 +0000</pubDate></item><item><title>Efficacy and Safety of Tildrakizumab for Treatment of Moderate-to-Severe Scalp Psoriasis in Patients with Obesity Over 52 Weeks.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/efficacy-and-safety-of-tildrakizumab-for-treatment-of-moderate-to-severe-scalp-psoriasis-in-patients-with-obesity-over-52-weeks-r610/</link><description><![CDATA[<h4>Introduction</h4>Obesity contributes to inflammation and may decrease psoriasis treatment efficacy. We investigated whether obesity affects the efficacy and safety of tildrakizumab, an anti-interleukin-23 p19 antibody approved for the treatment of adults with moderate-to-severe plaque psoriasis, for scalp psoriasis treatment.<h4>Methods</h4>This was a subgroup analysis of a randomized, double-blind, placebo-controlled, Phase 3b trial in patients with moderate-to-severe plaque psoriasis affecting the scalp. Patients receiving tildrakizumab 100 mg or placebo were analyzed by baseline obesity status (body mass index ≥ 30 versus &lt; 30 kg/m<sup>2</sup>). Efficacy outcomes included an Investigator Global Assessment (IGA) modified 2011 (scalp) (IGA mod 2011 [scalp]) score of "clear"/"almost clear" (0/1) with a ≥ 2-point reduction (IGA mod 2011 [scalp] response), ≥ 90% improvement in Psoriasis Scalp Severity Index (PSSI) score (PSSI 90 response), ≥ 4-point reduction in Scalp Itch-Numeric Rating Scale (Scalp Itch-NRS response; among patients scoring ≥ 4 at baseline), and percent change from baseline (%CFB) in affected scalp surface area (SSA). Safety was assessed from adverse events. The analysis was not prospectively powered to detect differences between subgroups.<h4>Results</h4>In the intention-to-treat population, 56/117 (47.9%) patients randomized to tildrakizumab and 57/114 (50.0%) to placebo had obesity (modified intention-to-treat population: tildrakizumab, 43/89 [48.3%]; placebo, 40/82 [48.8%]). At Week 16, significantly more patients treated with tildrakizumab versus those receiving placebo achieved IGA mod 2011 (scalp) (obesity, 21/43 [48.8%] versus 4/40 [10.0%], p = 0.0002; no obesity, 23/46 [50.0%] versus 2/42 [4.8%], p &lt; 0.0001) and PSSI 90 responses (obesity, 27/43 [62.8%] versus 4/40 [10.0%], p &lt; 0.0001; no obesity, 27/46 [58.7%] versus 0/42 [0.0%], p &lt; 0.0001). Treatment effect was also maintained for Scalp Itch-NRS response (p &lt; 0.0001) and mean %CFB in affected SSA (no statistical testing), regardless of obesity status. Results in patients treated with tildrakizumab were similar through Week 52. No new safety signals were identified.<h4>Conclusions</h4>No statistically significant differences in efficacy or safety were observed between patients with and without obesity.<h4>Clinicaltrials</h4><h4>Gov identifier</h4>NCT03897088.<p><a href="http://europepmc.org/article/MED/42105056?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">610</guid><pubDate>Thu, 14 May 2026 18:05:26 +0000</pubDate></item><item><title>The role of biosimilars in enhancing global access to psoriasis treatment.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/the-role-of-biosimilars-in-enhancing-global-access-to-psoriasis-treatment-r608/</link><description><![CDATA[The introduction of biosimilars for moderate-to-severe psoriasis treatment has demonstrated comparable efficacy and safety to originator biologics, with the potential to improve cost-effectiveness. We explored the potential for biosimilars to improve access to biologics for psoriasis, especially in low-and-middle-income countries where costs often limit access to originators. The analysis was based on a systematic review conducted as part of the submission process to include adalimumab and ustekinumab in the World Health Organization Essential Medicines List for psoriasis. Among 17 studies included in the systematic review, we focused on those that provided data evaluating the cost and/or cost-effectiveness of biosimilars versus originators in the treatment of psoriasis. Two studies met the inclusion criteria. The first was a cohort-based Markov model which showed that biosimilar adalimumab was cost-effective compared with originator adalimumab for moderate-to-severe psoriasis. The second, using a cost-per-responder model, found that adalimumab biosimilar had the lowest cost-per psoriasis area and severity index (PASI) complete clearance (PASI100) responder among the anti-tumor necrosis factor therapies. Biosimilars have a key role in reducing costs and expanding treatment availability for psoriasis patients. Further health economic studies, focusing on psoriasis, are required to demonstrate how biosimilars can improve access to biologics in this condition.<p><a href="http://europepmc.org/article/MED/42002071?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">608</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Identification and clinical implications of immune-related hub genes in psoriasis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/identification-and-clinical-implications-of-immune-related-hub-genes-in-psoriasis-r607/</link><description><![CDATA[<h4>Background</h4>Psoriasis, a chronic inflammatory skin disease affecting 2-3% of the global population, is driven by dysregulated immune responses. Despite advancements in biologic therapies, treatment challenges persist due to high recurrence rates. This study aimed to identify immune-related hub genes and elucidate their clinical implications in psoriasis pathogenesis and therapy.<h4>Methods</h4>Multiple microarray datasets from psoriasis patients (GSE30999, GSE106992, GSE14905, GSE78097, and GSE117468) were obtained to identify immune-key genes by differential gene analysis and Weighted Gene Co-expression Network Analysis (WGCNA). Subsequently, immune-related hub genes were identified using the Least Absolute Shrinkage and Selection Operator (LASSO) algorithm and Protein-Protein Interaction (PPI) networks, with further validation through Gene Set Enrichment Analysis (GSEA) and Receiver Operating Characteristic (ROC) curves to assess exploratory within-sample discrimination. Pearson correlation analysis evaluated the relationship between hub genes, skin lesion severity, and treatment outcomes. The study also conducted immune infiltration by using the Cell-type Identification by Estimating Relative Subsets Of RNA Transcripts (CIBERSORT) algorithm and identified potential therapeutic targets by the Drug-Gene Interaction Database (DGIdb).<h4>Results</h4>Thirty-one immune-related key genes were identified, and six hub genes (CLEC7A, CXCL1, IRF1, S100A12, S100A8, S100A9) were validated as central players in immune signaling pathways. These genes exhibited within-sample discrimination (AUC &gt; 0.9) and correlated with disease severity and biological therapy efficacy. Immune infiltration analysis revealed increased activated memory CD4+ T cells and M1 macrophages in lesional skin, which was strongly associated with hub gene expression. Additionally, drug-gene interaction analysis identified potential therapeutic agents targeting these genes.<h4>Conclusion</h4>This study identified six immune-related hub genes that were closely linked to the severity of psoriasis, the effectiveness of biological treatments, and infiltrated activated memory CD4+ T cells and M1 macrophages. Our findings elucidate a novel immune-related hub gene network in psoriasis and provide potential targets for the development and application of biologics.<p><a href="http://europepmc.org/article/MED/42008507?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">607</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Update on the Etiology and Pathogenesis of Erythrodermic Psoriasis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/update-on-the-etiology-and-pathogenesis-of-erythrodermic-psoriasis-r606/</link><description><![CDATA[Erythrodermic psoriasis(EP) is a rare, life-threatening variant affecting 75%-90% of the body surface area. Characterized by widespread erythema and potential systemic symptoms like fever and lymphadenopathy, it severely impairs patient quality of life. The pathogenesis of erythrodermic psoriasis is not fully understood. It is a multifactorial, multistep process suspected to result from an abnormal immune response induced by both genetic and environmental factors. Key contributors to erythrodermic psoriasis onset include specific gene polymorphisms, altered expression of adhesion molecules, dysregulated cytokine activity, and abnormal activation of T cell subsets. Additionally, imbalances in the skin microbiota and external factors, such as infections and medications, play important roles in disease onset and progression. Distinct from prior reviews that primarily emphasize clinical features and treatment, this review integrates recent mechanistic advances across genetic, immune, environmental, and microbiome domains to provide an updated, systems-level framework for understanding erythrodermic psoriasis and to highlight potential therapeutic implications.<p><a href="http://europepmc.org/article/MED/41982475?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">606</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Proliferation-associated protein 2G4 promotes keratinocyte proliferation and survival in psoriasis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/proliferation-associated-protein-2g4-promotes-keratinocyte-proliferation-and-survival-in-psoriasis-r605/</link><description><![CDATA[<h4>Background</h4>Psoriasis is a non-communicable inflammatory skin disease that affects approximately 2%-3% of the world's population. Given its high impact on quality of life and the fact that a subset of patients exhibits suboptimal or secondary loss of response to current treatments, identifying new therapeutic strategies is crucial. Proliferation-associated protein 2G4 (PA2G4) is a transcription factor that has been exclusively studied in cancer research, where it promotes cell growth and enhances tumourigenesis by inhibiting apoptosis. However, its role in inflammatory skin diseases remains largely unknown.<h4>Objectives</h4>This study focused on the pathophysiological and immunological functions of PA2G4 in psoriasis and evaluated its potential as a therapeutic target.<h4>Methods</h4>Bulk, single-cell, and spatial RNA sequencing combined with immunohistochemistry were used to assess PA2G4 expression in psoriatic skin compared with that in non-lesional controls. Functional studies were performed in primary human keratinocytes and reconstructed human epidermis (RHE) models using the CRISPR/Cas9-mediated knockout (KO) of PA2G4 and pharmacological inhibition of PA2G4 with the small-molecule WS6. The regulatory effects of PA2G4 on cellular processes, such as proliferation, differentiation, and survival, were investigated using RNA-seq, western blot analysis, scratch assays, and annexin V staining.<h4>Results</h4>PA2G4 was highly abundant in psoriasis, and its expression was predominantly restricted to basal proliferating keratinocytes. Its gene expression is positively correlated with psoriasis severity, the degree of acanthosis, neutrophil infiltration, and genes which are upregulated in psoriasis. PA2G4 KO in primary human keratinocytes activated differentiation pathways while suppressing proliferation pathways, resulting in the downregulation of proliferation- and inflammation-related genes (e.g. MKI67, IL20, VEGFA, and HIF1A) and the upregulation of differentiation and cell adhesion markers (e.g. KRT6C, LCE2C, and DSG4). Functionally, the PA2G4 KO reduced keratinocyte proliferation in scratch assays, attenuated interleukin-22-induced acanthosis in RHE models, and promoted keratinocyte death. Pharmacological inhibition of PA2G4 using the small-molecule inhibitor WS6 similarly downregulated genes associated with proliferation and cell survival.<h4>Conclusions</h4>PA2G4 could promote keratinocyte hyperproliferation and survival in psoriasis, thereby critically influencing epidermal homeostasis. Therefore, inhibition of PA2G4 may represent a new treatment option for psoriasis.<p><a href="http://europepmc.org/article/MED/42008715?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">605</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Retrospective Analysis of Inflammatory Parameters and Vitamins' Levels in Psoriasis Patients: A Case-Control Study.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/retrospective-analysis-of-inflammatory-parameters-and-vitamins-levels-in-psoriasis-patients-a-case-control-study-r604/</link><description><![CDATA[<h4>Introduction</h4>Psoriasis is a chronic immune-mediated inflammatory disorder affecting both adults and children worldwide, with an average prevalence of approximately 2%. Recent evidence suggests that several hematological inflammatory parameters and vitamin levels may serve as accessible biomarkers for disease activity and severity assessment.<h4>Methods</h4>This single-center retrospective case-control study was conducted at Jordan University Hospital using electronic medical record data from January 2019 to December 2023. The study included 142 patients with psoriasis and 277 age- and sex-matched controls. Psoriasis severity was assessed using the Psoriasis Area and Severity Index (PASI). Hematological inflammatory indices-including neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII)-as well as vitamin D and vitamin B12 levels were evaluated.<h4>Results</h4>The mean age ± standard deviation was 43.76 ± 16.78 years, with no significant differences between psoriasis cases and controls. Females accounted for 54.93% of psoriasis cases compared with 54.41% of controls. The mean PASI score was 9.02 ± 9.00. Approximately 51.79% of psoriasis patients were vitamin D deficient, while 17.82% had vitamin B12 deficiency. No significant differences in psoriasis severity categories were observed across vitamin B12 or vitamin D levels (p = 0.808 and p = 0.184, respectively). The mean NLR, PLR, and SII were 2.21, 124.6, and 588,441.8, respectively. These inflammatory indices did not demonstrate statistically significant differences between psoriasis patients and controls (p &gt; 0.05).<h4>Conclusion</h4>No significant associations were observed between psoriasis severity and inflammatory hematological indices (NLR, PLR, SII) or vitamin deficiencies. These findings suggest limited standalone utility of these biomarkers for routine assessment of psoriasis severity in this retrospective cohort.<p><a href="http://europepmc.org/article/MED/41993888?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">604</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Cell-type-specific causal effects of CEBPD in CD8&#x2009;+&#x2009;S100B&#x2009;+&#x2009;Tcells and ZFP36 in monocytes modulate the protective and risk phenotypes in psoriasis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/cell-type-specific-causal-effects-of-cebpd-in-cd8%E2%80%89%E2%80%89s100b%E2%80%89%E2%80%89tcells-and-zfp36-in-monocytes-modulate-the-protective-and-risk-phenotypes-in-psoriasis-r603/</link><description><![CDATA[Psoriasis is a chronic immune-mediated inflammatory skin disease characterized by dysregulated keratinocyte proliferation, immune cell infiltration, and systemic comorbidities. Despite the identification of numerous genetic susceptibility loci for psoriasis through genome-wide association studies (GWAS), their functional roles and underlying causal contributions to psoriasis pathogenesis remain largely unclear. Integrating multi-omics data with causal inference approaches, such as Mendelian randomization (MR), represents a promising strategy for addressing this gap and identifying key regulatory genes. We integrated transcriptome data from the Gene Expression Omnibus database (GEO) database (GSE14905 and GSE30999) and performed weighted gene co-expression network analysis and differential expression analysis to identify psoriasis-related genes. Protein-protein interaction networks and four centrality algorithms (Maximal Clique Centrality (MCC), Maximum Neighborhood Component (MNC), Edge Percolated Component (EPC), and Degree centrality) were applied to identify hub genes, and machine learning methods (least absolute shrinkage and selection operator regression, Random Forest, and artificial neural network) were used to screen diagnostic biomarkers. Immune infiltration analysis was performed using CIBERSORT, and the causal association of signature genes with psoriasis was examined using two-sample MR with single-cell expression quantitative trait locus data from the OneK1K cohort and GWAS summary statistics from FinnGen. Module genes that were significantly associated with psoriasis were identified in our study, among which 19 hub genes were screened. Using machine learning approaches, we further refined these findings to seven signature genes. The diagnostic model based on these seven genes achieved an area under the curve of 0.980. Immune infiltration analysis revealed strong associations between CCAAT/enhancer-binding protein delta (CEBPD) and activated CD4 + memory T cells and follicular helper T cells, and between zinc finger protein 36 (ZFP36) and M1 macrophages. MR analysis demonstrated that higher CEBPD expression in CD8 + S100B + T cells was protective (odds ratio [OR] = 0.795, P = 0.015), whereas higher expression of the ZFP36 gene in monocytes was a risk factor (OR = 1.214, P = 0.043) for psoriasis. Our study identified a robust seven-gene signature with high diagnostic accuracy for psoriasis and provided genetic evidence for the cell type-specific causal role of CEBPD and ZFP36. These findings enhance our understanding of psoriasis pathogenesis and suggest potential targets for developing cell-selective immunomodulatory therapies.<p><a href="http://europepmc.org/article/MED/41991682?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">603</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Wogonin attenuates psoriasis through anti-inflammatory effects by inhibiting reactive oxygen species production and the AKT/NF-&#x3BA;B signaling pathway.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/wogonin-attenuates-psoriasis-through-anti-inflammatory-effects-by-inhibiting-reactive-oxygen-species-production-and-the-aktnf-%CE%BAb-signaling-pathway-r602/</link><description><![CDATA[Psoriasis is a common, chronic, inflammatory skin disease that affects many patients and exerts a heavy physical and mental burden. Wogonin (WG), derived from the root extract of Scutellaria Baicalensis, has shown therapeutic effects in a variety of inflammatory diseases. However, its specific effects and mechanisms in psoriasis treatment remain poorly understood. This study aimed to investigate the therapeutic effects and underlying mechanisms of WG in psoriasis. In this study, we first identified potential therapeutic targets of WG for psoriasis by intersecting the corresponding targets of psoriasis and WG, then performed Protein-Protein Interaction (PPI) network analysis and enrichment analyses. Next, we employed Cytoscape to identify potential key targets and performed molecular docking to predict possible targets. M5-induced HaCaT cells and imiquimod (IMQ)-mouse models were used to explore the effects and mechanisms. Bioinformatic analyses indicated that WG may exert anti-inflammatory effects through inhibiting PI3K/AKT pathway activation and oxidative stress. In vitro results showed that WG suppressed the increase of pro-inflammatory cytokine expression levels, reactive oxygen species (ROS) level, phosphorylation of Akt and p65, and several key target mRNA expression levels induced by M5 stimulation. Oral administration of WG remarkably alleviated psoriatic like lesions in IMQ-induced mice, inhibited inflammatory cytokines and Ki-67 expression level in mouse skin lesions. Our results indicate that WG exhibits significant anti-inflammatory effects in psoriasis by suppressing reactive oxygen species (ROS) production and inhibiting the AKT/NF-κB signaling pathway. These results highlight WG's potential as a promising therapeutic agent for psoriasis treatment.<p><a href="http://europepmc.org/article/MED/42000881?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">602</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Role of the STAT3 Signaling Pathway in Cell Proliferation and Inflammation in Psoriasis and Approaches for Targeted Therapies: A Review.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/role-of-the-stat3-signaling-pathway-in-cell-proliferation-and-inflammation-in-psoriasis-and-approaches-for-targeted-therapies-a-review-r601/</link><description><![CDATA[Psoriasis is a common chronic inflammatory skin disease with a complex pathogenesis that involves the dysregulation of multiple cellular components and interconnected molecular pathways. Signal transducer and activator of transcription 3 (STAT3) is a key transcription factor that integrates signals from multiple cytokines and growth factors to regulate gene expression involved in cell proliferation, survival, and inflammation. Emerging evidence has shown the pivotal role of STAT3 in driving the persistent inflammatory state and aberrant keratinocyte behavior characteristic of psoriasis. This review systematically summarizes the fundamental biological functions of STAT3 (including its phosphorylation, dimerization, and nuclear translocation processes) and its intrinsic mechanism of action in the pathological process of psoriasis. We focus on the critical regulatory role of STAT3 in psoriasis-related inflammatory signaling networks, detailing how it modulates the expression of pro-inflammatory mediators to influence abnormal immune responses and pathological keratinocyte proliferation in lesional skin. Furthermore, the review comprehensively evaluates the latest developments in STAT3-based targeted therapeutic strategies, including small-molecule inhibitors (eg, WB518 and quinone derivatives), biologics, and nucleic acid-based approaches (eg, siRNA and miRNA delivery systems), analyzing their efficacy, safety profiles, and potential clinical applications in current and future treatment regimens. By synthesizing findings from numerous experimental and clinical studies, we aim to address the existing research gap regarding the precise specific regulatory mechanisms of STAT3 and its translational therapeutic implications in psoriasis, providing a foundation for the development of more effective and personalized therapeutic interventions for this condition.<p><a href="http://europepmc.org/article/MED/42015469?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">601</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>The Effectiveness of Probiotics in Psoriasis: An Umbrella Review.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/the-effectiveness-of-probiotics-in-psoriasis-an-umbrella-review-r600/</link><description><![CDATA[<h4>Background</h4>Psoriasis is an immune-mediated inflammatory skin condition that is chronic and causes a great deal of disease burden, especially for those affected in their most productive years. Gut microbiota, immune parameters and, in turn, psoriasis symptom improvement have recently been associated with the use of probiotics in several different studies.<h4>Objectives</h4>This study aims to conduct an umbrella review of systematic reviews and meta-analyses of the effectiveness of probiotic supplementation as a possible adjuvant in the treatment of psoriasis.<h4>Methods</h4>This umbrella review is listed in the PROSPERO database (registration number CRD420251130518) and was referenced according to the PRISMA 2020 guidelines. The data were obtained after a systematic search of the literature in Cochrane, Scopus and PubMed. The quality of the methodology was evaluated using the AMSTAR 2 tool; the overlap was evaluated with the corrected covered area (CCA) method.<h4>Discussions</h4>Five systematic reviews and meta-analyses were included, covering hundreds of adult psoriasis patients. The probiotics studied consisted of both single-strain and multistrain formulations, sometimes combined with prebiotics. Probiotics are associated with significantly reduced Psoriasis Area and Severity Index (PASI) scores, increased PASI 75 response rates, lowered inflammatory biomarkers (CRP, TNFα, IL-6) and improved Dermatology Life Quality Index (DLQI). Greater effectiveness was found with multistrain probiotics, treatment duration of ≥ 12 weeks and studies conducted in Asia. Most studies reported good safety and minimal side effects. However, a high overlap among included reviews was observed (CCA = 38.64%), which should be considered when interpreting the findings and their limitations.<h4>Conclusions</h4>Probiotics, particularly multistrain formulations, show potential as a safe and effective adjuvant therapy for reducing psoriasis severity and improving patient quality of life. Further clinical trials are needed to identify the most effective strains and optimal duration of treatment.<p><a href="http://europepmc.org/article/MED/42005309?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">600</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Nanotechnology advances for psoriasis treatment and future prospects.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/nanotechnology-advances-for-psoriasis-treatment-and-future-prospects-r599/</link><description><![CDATA[Psoriasis is a chronic, immune-mediated disorder with strong genetic susceptibility and environmental triggers, characterized by excessive proliferation of keratinocytes and recruitment of inflammatory cells. Affecting 2-3% of the global population and represents a significant public health challenge. In psoriasis, the skin barrier is altered rather than uniformly enhanced, and its permeability varies with drug types and disease states, which may affect the effective delivery of drugs to affected areas. Nanotechnology demonstrates potential in drug delivery, protecting drug molecules from degradation, enabling targeted therapy, and reducing side effects, thereby improving pharmacokinetics and enhancing the bioavailability of therapeutic agents. This review specifically examines the emergence of multimodal nanotherapeutic approaches, which defined as the strategic integration of two or more distinct therapeutic modalities (e.g., pharmacotherapy paired with phototherapy, gene editing, or RNA interference) within a unified nanocarrier platform to achieve synergistic efficacy. By systematically evaluating these advanced combinatory strategies, this review provides a distinct perspective compared to existing literature, which predominantly focuses on conventional, single-mode drug delivery systems. To this end, it reviews nanotechnology combined with multiple therapies and introduces the current advantages and disadvantages of integrating nanotechnology with conventional anti-psoriatic drugs Finally, it presents the challenges and prospects of using nanotechnology to treat psoriasis and provides reliable solutions for its clinical management. Overall, this review advances psoriasis treatment toward precision and efficiency, revealing the broad prospects of nanomedicine in conquering this intractable disease.<p><a href="http://europepmc.org/article/MED/41984395?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">599</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Majoon Ushba alleviated IL-17A sensitized keratinocyte ferroptosis via JAK-2-STAT-3 signaling axis and reversed imiquimod induced psoriasiform inflammation.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/majoon-ushba-alleviated-il-17a-sensitized-keratinocyte-ferroptosis-via-jak-2-stat-3-signaling-axis-and-reversed-imiquimod-induced-psoriasiform-inflammation-r598/</link><description><![CDATA[Psoriasis is a relapsing autoimmune disease exacerbated by aberrant interleukin (IL)-17 A activity. Majoon Ushba, a unani polyherbal formulation implicated in clinical cases of psoriasis lacks immunopharmacological validation. The study aims to investigate the pre-clinical efficacy of Majoon Ushba and its therapeutic role in mitigating IL-17A-induced keratinocytes ferroptosis via ablation of JAK-2/STAT-3 pathway. HaCaT cells were stimulated with IL-17A to assess the activation of the JAK-2-STAT-3 pathway. The STAT-3 inhibitor, S3I-201, was used to confirm the role of the STAT-3 axis in keratinocyte ferroptosis. Majoon Ushba pretreatment was assessed to determine its efficacy in alleviating keratinocyte ferroptosis. An imiquimod (IMQ)-induced psoriasis mouse model was used to evaluate the pre-clinical efficacy of Majoon Ushba. Furthermore, prior high-performance liquid chromatography (HPLC) profiling was leveraged for in-silico docking analysis to identify the binding affinities of key phytoconstituents with IL-17RA and STAT-3. Majoon Ushba alleviated the IL-17A/JAK-2-STAT-3 axis, improved GPX4 expression, and regulated lipid peroxidation. Subsequently, Majoon Ushba also reversed the expression of pathogenic mediators and led to a reduction in serum cytokine levels of IL-17A, IL-23, and IFN-γ. An in-silico docking analysis suggested favorable binding affinities for key phytoconstituents of Majoon Ushba against IL-17RA and STAT-3. Aligned with pre-clinical and in vitro results, the computational findings offer initial evidence that the polyherbal formulation may influence the IL-17A/JAK-2-STAT-3 signaling pathway. In conclusion, our preliminary findings reveal a plausible mechanistic basis for the anti-psoriatic efficacy of Majoon Ushba, warranting larger clinical trials in psoriasis patient cohorts.<p><a href="http://europepmc.org/article/MED/41973793?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">598</guid><pubDate>Tue, 14 Apr 2026 07:47:06 +0000</pubDate></item><item><title>Efficacy and safety of ustekinumab biosimilars for treating moderate-to-severe plaque psoriasis: a systematic review and network meta-analysis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/efficacy-and-safety-of-ustekinumab-biosimilars-for-treating-moderate-to-severe-plaque-psoriasis-a-systematic-review-and-network-meta-analysis-r597/</link><description><![CDATA[To compare the efficacy and safety of different ustekinumab biosimilars for treating moderate-to-severe plaque psoriasis (PP), providing an evidence-based basis for clinical medication. We systematically searched randomized controlled trials on ustekinumab biosimilars for treating moderate-to-severe PP in adults from Embase, PubMed, Cochrane Library, and Web of Science. Stata 18.0 was utilized for data analysis. Nine studies were included, involving 4293 moderate-to-severe PP patients. 1) Ustekinumab biosimilars and the reference listed drug (RLD) ustekinumab-RP had no significant difference in the psoriasis area and severity index (PASI) improvement (P &gt; 0.05), and the biosimilar CT-P43 was most effective in improving PASI at different time points. 2) For the dermatology life quality index, Bmab1200, AVT04 and CT-P43, had statistically significant differences from the RLD (P &lt; 0.05). 3) The biosimilar CT-P43 was most effective in improving the Physician Global Assessment score, with the highest SUCRA value (99.8%). 4) The reduction of the body surface area and the treatment-emergent adverse event rate had no statistically significant difference from the RLD (P &gt; 0.05). 5) The biosimilar CT-P43 and Bmab1200 demonstrated a lower probability of generating anti-drug antibodies, showing statistically significant differences from other biosimilars (P &lt; 0.05). Ustekinumab biosimilars demonstrate comparable efficacy and safety to ustekinumab-RP for treating moderate-to-severe PP in adults. The biosimilar CT-P43 is more effective in improving short-term PASI. Due to limitations in the number and quality of included studies, more high-quality studies are required to validate these findings.<p><a href="http://europepmc.org/article/MED/41957184?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">597</guid><pubDate>Tue, 14 Apr 2026 07:32:37 +0000</pubDate></item><item><title>AR and ITGAL: Key Mediators of Andrographis paniculata's Anti-Psoriatic Effects Revealed by Multi-Omics Analysis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/ar-and-itgal-key-mediators-of-andrographis-paniculatas-anti-psoriatic-effects-revealed-by-multi-omics-analysis-r596/</link><description><![CDATA[<h4>Introduction</h4>This study analyzed the mechanisms of action of Andrographis paniculata (AP), a medicinal plant with diverse pharmacological properties, on psoriasis.<h4>Materials and methods</h4>The active components of AP and their corresponding targets were identified. These targets were subsequently intersected with differentially expressed genes (DEGs) and immune-related genes associated with psoriasis. The resulting gene set was subjected to functional enrichment analysis and immune infiltration analysis. The scRNA-seq data were analyzed to delineate the single-cell landscape in psoriasis and cell type-specific expression of genes of interest. Further, the molecular docking and experimental verification were performed for validation.<h4>Results</h4>Active components of AP and their targets were predicted. Cross-referencing these targets with psoriasis DEGs revealed 2 feature genes (AR and ITGAL), both exhibiting strong diagnostic potential. The two genes were associated with differentially enriched pathways and immune cell infiltration. Further, scRNA-seq analysis identified 10 cell subclusters. Notably, AR was expressed in reticular fibroblasts of healthy controls, while ITGAL was expressed in T cells of psoriasis samples. Molecular docking confirmed a stable binding interaction between Dehydroandrographolide and AR. In vitro validation using an M5 cytokine-induced keratinocyte model demonstrated that Dehydroandrographolide exerted potent anti-inflammatory and antiproliferative effects. Furthermore, it significantly modulated the protein expression levels of both genes.<h4>Discussion</h4>Combining in-silico and in-vitro analyses, this study identified AR and ITGAL as potential key mediators and validated the efficacy of the active component of AP, Dehydroandrographolide, against psoriasis.<h4>Conclusion</h4>Collectively, the study demonstrated that AP had the potential anti-psoriasis effects.<p><a href="http://europepmc.org/article/MED/41968824?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">596</guid><pubDate>Tue, 14 Apr 2026 07:32:37 +0000</pubDate></item><item><title>Analysis of Clinical Characteristics and Treatment Needs in Elderly Patients with Psoriasis Vulgaris: A Single-Centered Retrospective Study.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/analysis-of-clinical-characteristics-and-treatment-needs-in-elderly-patients-with-psoriasis-vulgaris-a-single-centered-retrospective-study-r595/</link><description><![CDATA[<h4>Background</h4>Psoriasis is a chronic, immune-mediated skin disorder that causes physical, psychological, and social burdens. There is a growing need to better characterize the distinct clinical features and specific treatment needs of elderly patients with psoriasis, which remains an important area for further research to optimize care in this population.<h4>Objective</h4>To investigate the clinical characteristics, comorbidities, and treatment preferences of elderly patients with psoriasis vulgaris.<h4>Methods</h4>Patients with psoriasis vulgaris were included in this retrospective study. Data on demographics, disease characteristics, including age at diagnosis, body surface area (BSA), Psoriasis Area and Severity Index (PASI), Dermatology Life Quality Index (DLQI), comorbidities, and treatment needs were collected. Patients at the visit over 60 years of age were defined as elderly patients. Patients who were diagnosed before 40 years of age were defined as early-onset psoriasis (EOP), and patients who were diagnosed over 40 years of age were defined as late-onset psoriasis (LOP). Continuous variables were compared using t-tests or Mann-Whitney <i>U</i>-tests, categorical variables using Chi-square or Fisher's exact tests. Spearman correlation was used for association analysis. Statistical significance was set at <i>P</i>&lt;0.05.<h4>Results</h4>A total of 375 patients were included, comprising 70 (18.67%) elderly and 305 (81.33%) non-elderly patients. The elderly group had a significantly higher proportion of LOP (87.14% vs 48.76%, <i>P</i>&lt;0.05). A higher percentage of elderly patients had moderate-to-severe (27.14% vs 20.98%, <i>P</i>&lt;0.05) and severe (1.43% vs 0.66%, <i>P</i>&lt;0.05) disease. Comorbidities were more prevalent in the elderly, including cardiovascular disease (12.86% vs 3.93%, <i>P</i>&lt;0.05) and diabetes (12.86% vs. 1.31%, <i>P</i>&lt;0.05). Despite this, elderly patients reported lower DLQI scores (median 2.00 vs. 3.00, <i>P</i>&lt;0.05). Regarding treatment needs, elderly patients were less likely to prioritize reducing treatment costs (10.00% vs 20.98%, <i>P</i>&lt;0.05) and preventing disease recurrence (30.00% vs 44.26%,<i> P</i>&lt;0.05) compared to non-elderly patients. Within the elderly cohort, EOP patients exhibited more severe disease (median BSA: 3.00 vs 2.00; median PASI: 3.30 vs 0.80, <i>P</i>&lt;0.05), a higher rate of familial psoriasis (33.33% vs 4.92%, <i>P</i>&lt;0.05), and a greater demand for reducing treatment costs (33.3% vs 6.56%, <i>P</i>&lt;0.05) compared to LOP patients.<h4>Conclusion</h4>Elderly patients with psoriasis present a distinct clinical profile characterized by a high prevalence of late-onset disease, a significant comorbidity burden, and differing treatment priorities focused less on cost and recurrence. Despite the increased clinical severity, their perceived quality-of-life impact is lower. Besides, they report higher dissatisfaction linked to unmet needs in itch relief, drug safety, and long-term control. Within the elderly cohort, early-onset patients had more severe disease, stronger familial predisposition, and greater cost-related concerns. The findings highlight the necessity for age-specific, multidimensional management strategies for this population.<p><a href="http://europepmc.org/article/MED/41971650?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">595</guid><pubDate>Tue, 14 Apr 2026 07:32:37 +0000</pubDate></item></channel></rss>
