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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/?d=1</link><description>Neue Studien: Europe PMC</description><language>de</language><item><title>Musculoskeletal and nail ultrasound findings in children with psoriasis: a case-control study.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/musculoskeletal-and-nail-ultrasound-findings-in-children-with-psoriasis-a-case-control-study-r632/</link><description><![CDATA[<h4>Background</h4>Children with psoriasis can develop juvenile psoriatic arthritis. Musculoskeletal ultrasound is a helpful imaging modality in the early recognition of joint inflammation. This pilot study aims to describe clinical and subclinical joint and nail abnormalities in children with psoriasis.<h4>Methods</h4>Children with psoriasis and healthy controls underwent ultrasound examination of various joints, entheses, and nails. Using a standard acquisition protocol, images were obtained in both B-mode and PD-mode. Differences between psoriasis and control groups were examined.<h4>Results</h4>Fifteen psoriasis patients who were not on systemic therapy and did not have clinical signs of arthritis and thirteen age- and sex-matched healthy controls were enrolled. While patients with psoriasis demonstrated subclinical synovitis in the finger, knee, and ankle joints more frequently than the control group (p = 0.047), no statistically significant difference was observed in the comparison of each specific joint. PD positivity was detected at the entheses in two patients with psoriasis and at three entheseal sites of two healthy children. Nail ultrasound examination demonstrated significantly thicker nail beds (1.6 vs. 1.4 mm, p &lt; 0.001) and more frequent abnormal nail structure (70% vs. 21.2%, p &lt; 0.001) in the psoriasis group compared to control group while the thickness of the nail plate and nail matrix were similar. Type II nail morphology changes were the most frequently detected type according to the Wortsman classification. Positive PD-mode findings in the nail bed and nail matrix were more common in the control group (both p &lt; 0.001). Among the psoriasis cohort, nails with abnormal exam findings had significantly thicker nail plate (0.4 vs. 0.35 mm, p = 0.003) and nail bed (1.8 vs. 1.6 mm, p = 0.006) measurements compared to nails with normal examination.<h4>Conclusions</h4>Ultrasound is a useful tool for evaluating inflammatory joint and nail findings that may help delineate subclinical joint inflammation in children with psoriasis.<p><a href="http://europepmc.org/article/MED/42143389?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">632</guid><pubDate>Mon, 25 May 2026 08:01:40 +0000</pubDate></item><item><title>Alkannin ameliorates imiquimod-induced murine psoriasis by targeting MrgprX2-mediated mast cell activation.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/alkannin-ameliorates-imiquimod-induced-murine-psoriasis-by-targeting-mrgprx2-mediated-mast-cell-activation-r631/</link><description><![CDATA[Activated mast cells (MCs) are crucial effectors in the initiation and progression of psoriasis by secreting inflammatory mediators. The MC activation mediated by Mas-related G-protein-coupled receptor X2 (MrgprX2) has been implicated in psoriasis progression. However, the therapeutic strategies targeting MrgprX2 for psoriasis treatment remain less explored. Alkannin (Alk) is the main active component of the plant Arnebia euchroma and exhibits significant anti-inflammatory activities. However, in psoriasis, the effect of Alk on MCs and MrgprX2 remains elusive. In psoriatic mouse models, Alk alleviated epidermal hyperplasia, vascular dilation, and splenomegaly, regulated the Th17 to Treg cells ratio, and reduced the proinflammatory cytokine levels. In vitro analyses indicated that Alk inhibited β-hexosaminidase release, downregulated the expression of inflammation-related cytokines, and reduced intracellular Ca2+ levels in a MrgprX2-dependent manner. Moreover, SPR, CETSA, DARTS, and molecular docking assays revealed a direct interaction between Alk and MrgprX2, suggesting that Alk targets MrgprX2 to inhibit MC activation. Furthermore, Alk inhibited the downstream PLCγ-IP3R-PKC-ERK signaling pathways via targeting MrgprX2. Consistently, in vivo functional assays confirmed that Alk inhibits MrgprB2-related MC activation, a critical process driving psoriatic symptom progression. Collectively, these results demonstrate that Alk directly binds to MrgprX2 and modulates MC activation by inhibiting downstream PLCγ-IP3R-PKC-ERK signaling pathways, thus mitigating psoriasis symptoms. These findings provide a novel target and theoretical basis for the treatment of psoriasis.<p><a href="http://europepmc.org/article/MED/42176861?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">631</guid><pubDate>Mon, 25 May 2026 08:01:40 +0000</pubDate></item><item><title>Feasibility of Ultrashort Echo Time MR Imaging for the Detection of Subclinical Achilles Enthesitis in Psoriasis and Psoriatic Arthritis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/feasibility-of-ultrashort-echo-time-mr-imaging-for-the-detection-of-subclinical-achilles-enthesitis-in-psoriasis-and-psoriatic-arthritis-r630/</link><description><![CDATA[Subclinical inflammation (SI) is clinically relevant in psoriasis (PsO) and psoriatic arthritis (PsA), but quantitative imaging biomarkers are lacking. We evaluated the feasibility of ultrashort echo time (UTE) bicomponent MRI for quantifying Achilles enthesis SI. Conventional MRI showed no group differences, whereas short T2* (T2*<sub>s</sub>) values were significantly elevated in PsO/PsA compared with healthy volunteers. These findings support the feasibility of UTE bicomponent analysis, as a promising tool for evaluating SI and warrant further investigation.<p><a href="http://europepmc.org/article/MED/42161535?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">630</guid><pubDate>Mon, 25 May 2026 08:01:40 +0000</pubDate></item><item><title>Durability of response to icotrokinra for high-impact site psoriasis: 1-year ICONIC-TOTAL findings.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/durability-of-response-to-icotrokinra-for-high-impact-site-psoriasis-1-year-iconic-total-findings-r629/</link><description><![CDATA[High-impact site plaque psoriasis is difficult to treat. Icotrokinra, an oral peptide with high specificity for the interleukin (IL)-23 receptor, demonstrated significantly higher rates of high-impact site psoriasis clearance, versus placebo, with no safety signals, through Week (W)16. Report clinical response rates and safety through 1 year of icotrokinra treatment in participants with high-impact site plaque psoriasis. Participants (≥12 years of age; psoriasis body surface area ≥1%; Investigator's Global Assessment [IGA] ≥2) with at least moderate scalp, genital or hand/foot psoriasis were randomized (2:1) to once-daily icotrokinra 200 mg (N = 208) or placebo (N = 103), with placebo-to-icotrokinra transition at W16 (N = 92). Rates (using nonresponder imputation) of achieving clear/almost clear (0/1) or clear (0) overall skin (IGA), genital (static Physician's Global Assessment of genitalia [sPGA-G]), hand/foot (hf-PGA) psoriasis and absent/very mild (0/1) or absent (0) scalp psoriasis (scalp-specific-IGA [ss-IGA]), modified Nail Psoriasis Severity Index (mNAPSI) percent improvement and safety were assessed through W52. Eighty-eight per cent (275/311) of participants completed treatment through W52. In icotrokinra-randomized participants, response rates increased through W24 and were durable through W52 for overall psoriasis clearance (IGA 0/1 range: 67%-70%) and across high-impact sites (ss-IGA 0/1: 72%-78%; sPGA-G 0/1: 85%-90%; hf-PGA 0/1: 54%-62%); responses were consistent among placebo-randomized participants after transitioning to icotrokinra. High proportions of icotrokinra-randomized participants achieved complete clearance during W24-52 (IGA 0: 44%-51%; ss-IGA 0: 57%-66%; sPGA-G 0: 73%-84%; hf-PGA 0: 44%-58%). Mean mNAPSI improvement increased from W16 (33%) to W52 (62%). Exposure-adjusted rates of participants with ≥1 adverse event (AE) or serious AE through W16 were similar between icotrokinra and placebo, with no increase in AE rates or occurrence of a safety signal through W52. Icotrokinra demonstrated high and durable rates of psoriasis clearance across high-impact sites, with a favourable safety profile, through 1 year.<p><a href="http://europepmc.org/article/MED/42175814?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">629</guid><pubDate>Mon, 25 May 2026 08:01:40 +0000</pubDate></item><item><title>Drug-induced psoriasis following sacubitril/valsartan: a case report and literature review.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/drug-induced-psoriasis-following-sacubitrilvalsartan-a-case-report-and-literature-review-r628/</link><description><![CDATA[Drug exposure is one of the potential mechanisms implicated in the onset or exacerbation of psoriasis. To date, several cardiovascular agents have been implicated. Sacubitril/valsartan (SV) has been widely used in the treatment of hypertension and heart failure (HF). Its common adverse reactions include angioedema, hypotension, renal impairment, and hyperkalemia. However, SV may cause psoriasis, which needs clinical attention. This report describes a case of a middle-aged male patient who developed psoriasis following SV therapy. The rashes presented as well-demarcated red or violaceous plaques with noticeable scaling. After being diagnosed with psoriasis, he was started on topical clobetasol propionate ointment, and SV was discontinued and replaced with ramipril for blood pressure control. During follow-up, the skin lesions showed marked improvement. However, the patient developed similar cutaneous manifestations again when SV was re-administered. He had previously developed psoriasis while using nifedipine, but transitioned to olmesartan and subsequently improved significantly with topical medication. Sacubitril enhances the effect of natriuretic peptides, which may be accompanied by a compensatory increase in angiotensin Ⅱ (Ang Ⅱ) levels, possibly contributing to the psoriasis. To the best of our knowledge, this is the first reported case worldwide of psoriasis potentially associated with SV, and the underlying mechanism appears likely to be related to sacubitril. It serves as a caution for clinicians prescribing SV, particularly in patients with a history of psoriasis or positivity for the HLA-Cw*0602 allele. Further studies are warranted to confirm the mechanism by which sacubitril induces psoriasis.<p><a href="http://europepmc.org/article/MED/42177422?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">628</guid><pubDate>Mon, 25 May 2026 08:01:40 +0000</pubDate></item><item><title>Association of Body Roundness Index, Lipid Accumulation Product, and Triglyceride-Glucose Index With Psoriasis: A Systematic Review of Observational Studies.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/association-of-body-roundness-index-lipid-accumulation-product-and-triglyceride-glucose-index-with-psoriasis-a-systematic-review-of-observational-studies-r627/</link><description><![CDATA[<h4>Background and aims</h4>Lipid dysregulation plays a crucial role in psoriasis pathogenesis and its cardiometabolic comorbidities. Novel anthropometric indices such as Body Roundness Index (BRI), Lipid Accumulation Product (LAP), and Triglyceride-Glucose (TyG) index have been proposed to better reflect underlying metabolic dysfunction and may be associated with psoriasis risk, severity, and related complications. This systematic review evaluates the current evidence on the associations of BRI, LAP, and the TyG index with psoriasis and related clinical outcomes.<h4>Methods</h4>A comprehensive literature search was conducted from inception up to September 2025. Observational studies examining the relationship between BRI, LAP, or TyG index and psoriasis or its clinical outcomes were included. Data synthesis comprised qualitative and descriptive statistical analyses.<h4>Results</h4>Fifteen studies comprising 65,130 participants from diverse countries met the inclusion criteria. Higher LAP was consistently associated with increased psoriasis risk but showed weak or no correlation with disease severity (PASI). All BRI studies, primarily using US National Health and Nutrition Examination Survey data, demonstrated a positive association between BRI and psoriasis risk, with modest predictive ability (AUC 0.56-0.58). TyG index was linked to adverse metabolic and cardiovascular outcomes, fatty liver disease, and all-cause mortality in psoriasis patients, although correlations with PASI were generally non-significant.<h4>Conclusions</h4>BRI, LAP, and TyG index are consistently associated with psoriasis risk and related metabolic and cardiovascular complications, highlighting their potential utility for early risk stratification and holistic management of psoriasis patients. Further prospective studies are warranted to clarify their predictive value for disease severity and long-term outcomes.<p><a href="http://europepmc.org/article/MED/42157919?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">627</guid><pubDate>Mon, 25 May 2026 08:01:40 +0000</pubDate></item><item><title>Novel post-translational modification learning signature reveals DPP3 promotes progression of psoriasis by enhancing inflammatory activation.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/novel-post-translational-modification-learning-signature-reveals-dpp3-promotes-progression-of-psoriasis-by-enhancing-inflammatory-activation-r626/</link><description><![CDATA[Although post-translational modifications (PTMs) significantly influence the pathogenesis of psoriasis, their specific mechanisms remain poorly understood. This study aimed to identify novel PTM-targeted therapeutic avenues for the precision treatment of psoriasis. Nine psoriasis-related datasets GSE13355, GSE14905, GSE30999, GSE41664, GSE51440, GSE53552, GSE54456, GSE117239, and GSE226244 were obtained. Consensus clustering was performed to identify psoriasis subtypes. Then, the study proceeded to pinpoint module genes by leveraging WGCNA. Additionally, the investigation also focused on uncovering hub genes by machine learning. Finally, we investigated the expression and localization of DPP3. A total of 2,141 differentially expressed genes (DEGs) were identified between the control and psoriasis samples. Enrichment analyses revealed that these DEGs are associated with inflammatory pathway involved in the progression of psoriasis. Additionally, two distinct psoriasis subclasses were identified, namely cluster.A and cluster.B. Moreover, 279 module genes related to these subtypes were identified using WGCNA. Then, utilizing the shared DEGs, cluster DEGs, key module genes, and PTM genes, 7 hub genes were obtained. Multiple machine learning models screened 7 key genes, demonstrated excellent diagnostic ability in psoriasis across multiple datasets (Average AUC = 0.901), and outperformed currently utilized diagnostic indicators specific to psoriasis. From a biological standpoint, the analysis revealed significant correlations between PTM.score and various inflammatory parameters. Notably, DPP3 emerged as an essential molecular element, exhibiting higher expression levels in psoriasis. Mechanistically, the overexpression of DPP3 enhances inflammatory activation, which in turn promotes the progression of psoriasis. This research provides genetic evidence supporting the therapeutic potential of targeting DPP3 in the treatment of psoriasis, while also elucidating its underlying pathophysiological mechanisms.<p><a href="http://europepmc.org/article/MED/42173459?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">626</guid><pubDate>Mon, 25 May 2026 08:01:40 +0000</pubDate></item><item><title>Studying the expression levels of LncRNA-MEG3 and miR-147b in the serum of psoriasis patients with and without dyslipidemia.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/studying-the-expression-levels-of-lncrna-meg3-and-mir-147b-in-the-serum-of-psoriasis-patients-with-and-without-dyslipidemia-r625/</link><description><![CDATA[Psoriasis is a chronic systemic inflammatory skin disorder that is strongly associated with metabolic disorders, including obesity, insulin resistance, hypertension, and dyslipidemia. Dyslipidemia causes abnormalities in lipid profiles, such as elevated triglycerides or low density lipoprotein (LDL) levels. Measure maternally expressed gene 3 (MEG3) and microRNA-147b in serum of patients with and without dyslipidemia compared to healthy control. These measurements were compared with clinical characteristics, clinical parameters, and laboratory investigations. Serum expression levels of MEG3 and microRNA-147b, as non-coding RNA biomarkers, were measured across four equally subcategorized groups (patients with and without dyslipidemia (N = 66) and healthy controls with and without dyslipidemia (N = 66) using Polymerase Chain Reaction (PCR). Psoriatic patients exhibited a high significantly body mass index and elevated low-density lipoprotein levels compared with controls (p = 0.038,0.010) respectively, while fasting blood glucose was significantl at p = 0.001. Fasting blood glucose and lipid parameters showed low levels in patients without dyslipidemia and high levels of high-density lipoprotein than those with dyslipidemia. Expression Level of MEG3 was significantly downregulated, whereas microRNA-147b was markedly upregulated in psoriatic patients (p &lt; 0.0001). MEG3 expression was negatively correlated with disease severity indices and lipid levels and inversely correlated with microRNA-147b, which also negatively correlated with disease duration. MEG3 and miR-147b, as non-coding RNAs, may show differential expression among psoriasis patient subgroups and could be associated with disease-related parameters, but their value as markers of disease severity or prognosis remains to be confirmed.<p><a href="http://europepmc.org/article/MED/42156472?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">625</guid><pubDate>Mon, 25 May 2026 08:01:40 +0000</pubDate></item><item><title>Correction: Association between Life's Essential 8 and psoriasis in US adults: a cross-sectional study</title><link>https://www.psoriasis-news.de/articles.html/1_articles/correction-association-between-lifes-essential-8-and-psoriasis-in-us-adults-a-cross-sectional-study-r624/</link><description><![CDATA[<small>No abstract supplied.</small><p><a href="http://europepmc.org/article/PMC/PMC13188854?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">624</guid><pubDate>Mon, 25 May 2026 08:01:40 +0000</pubDate></item><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></channel></rss>
