Experimental Dermatology最新文献

{"title":"LC-OCT for Cutaneous Lupus Erythematosus: Characterization Across Disease Subtypes and Differentiation From Rosacea","authors":"Daniele Omar Traini,&nbsp;Gerardo Palmisano,&nbsp;Rebecca Ventura,&nbsp;Maria Vittoria Cannizzaro,&nbsp;Clara De Simone,&nbsp;Pierluigi Rizzuti,&nbsp;Viviana Antonella Pacucci,&nbsp;Pier Giacomo Cerasuolo,&nbsp;Silvia Piunno,&nbsp;Cesare Gavotti,&nbsp;Mariarita Vigilante,&nbsp;Alessio Maccari,&nbsp;Giacomo Caldarola,&nbsp;Augusta Ortolan,&nbsp;Mariano Suppa,&nbsp;Alessandro Di Stefani,&nbsp;Maria Antonietta D' Agostino,&nbsp;Ketty Peris","doi":"10.1111/exd.70337","DOIUrl":"10.1111/exd.70337","url":null,"abstract":"<p>Cutaneous lupus erythematosus (CLE) encompasses a heterogeneous group of autoimmune skin manifestations that often overlap clinically with other inflammatory dermatoses, particularly rosacea. While histopathology remains the gold standard, its invasiveness limits routine and longitudinal use. Line-field confocal optical coherence tomography (LC-OCT) is an emerging non-invasive imaging modality capable of providing real-time, near-histological resolution of skin architecture. In this single-center cross-sectional observational study, 45 patients (30 CLE: 16 acute, 5 subacute, 9 chronic; 15 rosacea) underwent LC-OCT imaging of active lesions. Images were independently evaluated using predefined criteria reflecting histopathological features. LC-OCT identified key histopathological correlates of CLE in vivo. Interface dermatitis features (including dermoepidermal junction disruption, basal cell vacuolization and band-like inflammatory infiltrate) were highly prevalent in ACLE and SCLE, while chronic CLE was characterized by epidermal atrophy, hyperkeratosis, fibrosis and adnexal destruction. In contrast, rosacea exhibited a vascular and folliculocentric pattern with frequent peri-adnexal inflammation and Demodex infestation, without interface changes. Interobserver agreement was substantial to excellent for most criteria. In the ACLE versus rosacea comparison, interface dermatitis features like band-like DEJ infiltrate, DEJ disruption, basal vacuolization and apoptotic bodies were associated with ACLE. Conversely, rosacea exhibited a vascular-folliculocentric profile with peri-infundibular infiltrates and Demodex mites. In conclusion, LC-OCT enables non-invasive visualization of disease-specific microarchitectural patterns in CLE, reflecting both inflammatory and chronic remodelling changes. In this pilot study, it shows potential in differentiating CLE from rosacea and may support diagnosis, staging and treatment monitoring in clinical practice. Larger, multicenter studies are required to confirm the role of LC-OCT in the non-invasive diagnosis of CLE.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 8","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13430679/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148663539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Repetin Regulates Epidermal Barrier Homeostasis and Is Associated With Inflammatory Skin Diseases","authors":"Megumi Mizawa,&nbsp;Teruhiko Makino,&nbsp;Keita Takemoto,&nbsp;Shohei Kitayama,&nbsp;Seiji Yamamoto,&nbsp;Tadamichi Shimizu","doi":"10.1111/exd.70336","DOIUrl":"10.1111/exd.70336","url":null,"abstract":"<div>\u0000 \u0000 <p>Repetin (RPTN) is a member of the fusion S100 protein family encoded within the epidermal differentiation complex. Although genetic studies have revealed that RPTN is a susceptibility gene for atopic dermatitis (AD), its biological function remains poorly understood. In this study, we investigated the role of RPTN in epidermal homeostasis and inflammatory skin diseases. We examined RPTN expression in normal skin, inflammatory skin diseases, and differentiated normal human keratinocytes (NHKs). Functional analyses were performed using RPTN knockdown (KD) NHK and three-dimensional (3D) skin-equivalent models. Epidermal barrier function was assessed using a lucifer yellow permeability assay, and cytokine-mediated regulation of RPTN expression was evaluated using 3D atopic dermatitis (AD) and psoriasis models. RPTN was primarily expressed in the granular layer of the normal epidermis and increased with keratinocyte differentiation. In the 3D skin-equivalent model, RPTN deficiency impaired epidermal barrier function and induced the expression of differentiation-related genes, including FLG, IVL, TGM1, CLDN1, KLK7, ALOX12, and TCHHL1. Notably, RPTN knockdown significantly increased IL-25 expression. RPTN expression was elevated in chronic atopic dermatitis (AD) lesions and in hypergranular epithelia of psoriasis vulgaris, lichen planus, and epidermolytic ichthyosis. In a 3D AD model, IL-4 and IL-13 significantly induced RPTN expression. These findings indicate that RPTN contributes to maintaining epidermal barrier homeostasis and suggest that it may be associated with regulating inflammatory responses.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 8","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148663566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dermoscopic-Pathologic Correlates of Invasiveness and Nevus Visibility in Nevus-Associated Melanoma","authors":"Marco Spadafora,&nbsp;Erica Baschieri,&nbsp;Simonetta Piana,&nbsp;Shaniko Kaleci,&nbsp;Giacomo Santandrea,&nbsp;Giovanni Pellacani,&nbsp;Caterina Longo","doi":"10.1111/exd.70333","DOIUrl":"https://doi.org/10.1111/exd.70333","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <p>Nevus-associated melanoma (NAM) is histologically defined by coexisting nevus and melanoma components, yet the nevus component is frequently not visible on dermoscopy.</p>\u0000 \u0000 <p>We performed a retrospective, single-centre observational study including histologically diagnosed NAMs (2011–2024). Dermoscopic images were assessed independently by two readers. Histopathology was systematically revised to quantify nevus proportion, size, and depth. Univariate and multivariable logistic regression evaluated associations with (a) invasive vs. in situ NAM and (b) dermoscopically visible vs. non-visible nevus component.</p>\u0000 \u0000 <p>Among 340 NAMs, 36.8% were in situ and 63.2% invasive. A dermoscopic nevus was visible in 45.6%. In multivariable analysis, nevus visibility under dermoscopy was independently associated with histopathologic features such as larger nevus size, particularly 2.1–4 mm (OR 2.5, 95% CI 1.3–4.6), 4.1–10 mm (OR 3.7, 95% CI 2.0–7.0), and &gt; 10 mm (OR 5.3, 95% CI 1.4–20.0), whereas deep nevus location (OR 0.3, 95% CI 0.2–0.5) and ulceration (OR 0.2, 95% CI 0.1–0.6) reduced visibility. Invasive NAM was independently associated with a visible nevus component under dermoscopy (OR 2.5, 95% CI 1.7–3.7), shiny white structures (OR 5.0, 95% CI 2.6–9.4), negative pigment network (OR 1.9, 95% CI 1.2–3.2), and blue-white veil (OR 8.3, 95% CI 4.5–15.4), whereas atypical pigment network and melanoma pigmentation were inversely associated with invasion.</p>\u0000 \u0000 <p>Dermoscopic nevus visibility in NAM is mainly determined by nevus size and depth, while melanoma-related changes, particularly ulceration, can obscure the nevus component. Dermoscopic markers of invasiveness should prompt timely management even when an associated nevus is suspected.</p>\u0000 </section>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 8","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70333","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148616798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Minoxidil Sulfate Regulates JAK/STAT Signalling and Mitochondrial Function in Alopecia Areata","authors":"Jung-Min Shin,&nbsp;Bogyeong Go,&nbsp;Kyung Eun Jung,&nbsp;Chang Deok Kim,&nbsp;Young-Joon Seo,&nbsp;Young Lee","doi":"10.1111/exd.70335","DOIUrl":"10.1111/exd.70335","url":null,"abstract":"<p>Alopecia areata (AA) is an autoimmune hair disorder characterized by interferon-gamma (IFN-γ)–driven inflammation and collapse of hair follicle immune privilege. Although Janus kinase (JAK) inhibitors are effective, incomplete or delayed responses remain common. Minoxidil is frequently combined with JAK inhibitors in clinical practice, yet its immunomodulatory mechanisms in AA are unclear. We investigated the effects of minoxidil sulfate (MXS) on inflammatory signalling, immune privilege–associated features and mitochondrial stress responses, and evaluated whether MXS enhances the anti-inflammatory effects of the JAK inhibitor baricitinib. Clinical observations of patients receiving combination therapy were descriptively assessed. Mechanistic studies were conducted in human outer root sheath (ORS) cells stimulated with IFN-γ and polyinosinic:polycytidylic acid to model the AA inflammatory microenvironment. Representative clinical observations suggested accelerated hair regrowth after addition of oral minoxidil to baricitinib. In inflamed ORS cells, MXS enhanced baricitinib-mediated suppression of STAT1 phosphorylation and IFN-γ–inducible chemokines (CXCL9, CXCL10, CXCL11). MXS also exerted baricitinib-independent anti-inflammatory effects by inhibiting STAT1 and STAT3 activation. Furthermore, MXS reduced inflammatory induction of MHC class I expression and partially restored insulin-like growth factor-1 expression. MXS attenuated cytosolic and mitochondrial reactive oxygen species accumulation, mitochondrial DNA damage and loss of mitochondrial membrane potential, accompanied by suppression of NOX1 and NOX4 expression. These findings suggest that MXS modulates inflammatory signalling, preserves immune privilege–associated features and protects mitochondrial integrity, providing a mechanistic rationale for adjunctive use with JAK inhibitors without additional systemic immunosuppression.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 8","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70335","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148600457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Itraconazole in Low-Risk Basal Cell Carcinoma: Stabilisation Before Downstaging","authors":"Haohao Wan,&nbsp;Gen Quan","doi":"10.1111/exd.70327","DOIUrl":"10.1111/exd.70327","url":null,"abstract":"","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 7","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148430358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Possible Role of Mycobiome in the Pathophysiology of Acne: Structured Narrative Review and Perspectives","authors":"Delphine Kerob,&nbsp;Samir Salah,&nbsp;Susi Elaine Dal Belo,&nbsp;James Odeimi,&nbsp;Cecile Clavaud,&nbsp;Ann'Laure Demessant-Flavigny","doi":"10.1111/exd.70308","DOIUrl":"10.1111/exd.70308","url":null,"abstract":"<p>Acne vulgaris pathogenesis involves complex interactions between sebum hypersecretion, follicular hyperkeratinisation, microbial colonisation and inflammatory cascades. While the bacterial microbiome has been extensively studied, the role of the skin mycobiome, particularly lipophilic Malassezia species, remains less clearly defined in acne-prone sites. To evaluate evidence for skin mycobiome involvement in acne pathogenesis, a structured narrative review was conducted in PubMed/MEDLINE and PMC, synthesising findings from 14 cross-sectional studies involving 1650 participants from diverse geographic and ancestry backgrounds. Across sequencing and culture-based studies, <i>Malassezia</i> was the dominant fungal genus on healthy as well as acne-prone skin; species-level data most often identified <i>M. restricta</i> and <i>M. globosa</i>, with occasional reports of <i>M. furfur</i>. Although significant variations were observed in fungal abundance, discrepancies exist between studies due to differences in study design, sampling methods (surface swabs vs. comedone or pustule contents vs. pore strips), culture media (lipid-supplemented vs. standard), molecular target (ITS1 rDNA vs. other loci) and population demographics. Multiple sequencing studies did not detect significant fungal alpha/beta-diversity differences between acne and non-acne skin while confirming <i>Malassezia</i> species dominance. One study highlighted the potential underdiagnosis of <i>Malassezia</i> folliculitis in acne patients, suggesting that misdiagnosis may occur due to overlapping clinical presentations. Future studies should predefine primary outcomes, adjust for multiplicity, report sampling depth (surface vs. follicular), specify fungal rDNA region sequenced, use specific lipid-supplemented media for <i>Malassezia</i> isolation when culturing, co-profile bacteria and fungi, and add systematic clinical assessment of <i>Malassezia</i> folliculitis.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 7","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70308","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differentiation of Palmoplantar Psoriasis, Palmoplantar Pustulosis and Hyperkeratotic Palmoplantar Eczema Using Proteomic Analysis of Tape Strip Samples","authors":"Mila B. Johansen,&nbsp;Sule Altintas,&nbsp;Mariana Bronze,&nbsp;Anders Woetmann,&nbsp;Claus Zachariae,&nbsp;Charlotte Näslund-Koch,&nbsp;Marianne B. Løvendorf,&nbsp;Lone Skov","doi":"10.1111/exd.70318","DOIUrl":"10.1111/exd.70318","url":null,"abstract":"<p>Palmoplantar inflammatory dermatoses, including hyperkeratotic palmoplantar eczema (HPE), palmoplantar psoriasis (PP) and palmoplantar pustulosis (PPP), present overlapping clinical features that complicate diagnosis and limit targeted therapy. This prospective observational study evaluated whether minimally invasive tape strip sampling, combined with targeted proteomics, can distinguish these conditions at a molecular level. Adults with HPE (<i>n</i> = 14), PP (<i>n</i> = 10), and PPP (<i>n</i> = 12) were enrolled, and tape strips from esional and non-lesional skin were analysed using the Olink Reveal panel (1034 proteins) with validation by MSD multiplex immunoassays. Differentially expressed proteins, pathway enrichment analysis, and protein–protein interaction analyses were conducted across the three diseases, and longitudinal analyses were conducted in a subset of patients with PP. Protein expression patterns showed partial separation of PPP from PP and HPE, whereas PP and HPE overlapped. Lesional samples across all three diagnoses exhibited increased expression of inflammatory proteins compared with non-lesional skin. PPP showed a distinct molecular profile from PP and HPE, with enriched pathways related to neutrophil degranulation, innate immune activation, and Th17-associated signalling networks centred on IL-17A and CXCL8. No proteins were significantly differentially expressed between PP and HPE lesions. PP and HPE showed overlapping interferon-associated chemokines CXCL10-11, consistent with a shared inflammatory module. Inflammatory protein levels decline with clinical improvement in longitudinal PP samples. Overall, tape strip-based targeted proteomics is a feasible approach for palmoplantar diseases, revealing a distinct inflammatory signature that differentiates PPP from PP and HPE, although discrimination between PP and HPE remains limited.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 7","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70318","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MFAP4 Promotes Scar Formation by Regulating Macrophage-Myofibroblast Transformation Through Activation of the TGF-β/Smad3 Signalling Pathway","authors":"Zhu Zhu,&nbsp;Jing Dai,&nbsp;Jinglin Li,&nbsp;Mengyao Zhang,&nbsp;Chao Liu,&nbsp;Jiaxiong Hu,&nbsp;Chufeng Jiang,&nbsp;Jingpei Wang,&nbsp;Youhua Peng","doi":"10.1111/exd.70314","DOIUrl":"10.1111/exd.70314","url":null,"abstract":"<div>\u0000 \u0000 <p>Hypertrophic scar is a pathological consequence of abnormal wound healing, marked by excessive fibroblast proliferation and extracellular matrix (ECM) accumulation. Macrophage-to-myofibroblast transformation (MMT) plays a key role in this process, but its regulatory mechanisms remain under investigation. This study found that microfibril-associated protein 4 (MFAP4) is significantly upregulated in mice scar tissue and is closely associated with the MMT process. In a mouse excision injury model, knockdown of MFAP4 in vivo macrophages using adeno-associated virus (AAV)-mediated RNA interference significantly reduced dermal thickening and disorganized collagen fibre deposition in mice scar tissues. Macrophage infiltration, expression of the myofibroblast marker α-SMA, and the proportion of MMT cells (F4/80⁺α-SMA⁺) were shown to be remarkably reduced. In vitro, TGF-β1 induces elevated MFAP4 expression within mouse-derived bone marrow-derived macrophages (BMDMs) and promotes MMT. MFAP4 knockdown inhibits TGF-β1-induced myofibroblast transformation and expression of ECM synthesis-related molecules (α-SMA, Col-I and Vimentin), while MFAP4 overexpression enhances these effects. Mechanistic studies suggest that MFAP4 regulates this process via the TGF-β/Smad3 signalling activation. MFAP4 promotes Smad3 phosphorylation (p-Smad3), and overexpression of Smad3 in MFAP4-knockdown mouse-derived BMDMs reverses the inhibitory effects of MFAP4 deficiency on MMT and ECM synthesis. These results reveal a key role for the MFAP4-TGF-β/Smad3 axis in regulating MMT-driven scar formation, providing novel insights into the mechanisms of hypertrophic scarring in mice and underlying therapeutic targets for clinical intervention.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 7","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reducing Unmet Needs in Hidradenitis Suppurativa by Including the Hair Follicle Among an Arsenal of Targets","authors":"Kyle Maas,&nbsp;Olivia D. Perez,&nbsp;Sarah E. Millar,&nbsp;Miriam K. Pomeranz,&nbsp;Lynn Petukhova","doi":"10.1111/exd.70321","DOIUrl":"10.1111/exd.70321","url":null,"abstract":"<p>Hidradenitis suppurativa (HS) is a prevalent, debilitating disease affecting ~1% of the population, with limited therapeutic options and poor long-term remission rates. HS arises from inflammation and destruction of apocrine-bearing hair follicles, suggesting a multifactorial pathology involving immune dysregulation and follicular dysfunction. Emerging treatment strategies largely center on immune suppression, with three FDA-approved therapies targeting inflammatory pathways. However, most patients fail to achieve durable remission. Genetic evidence increasingly implicates the hair follicle as a key contributor to HS pathogenesis. For example, genes that cause ectodermal dysplasias (EDs) have been implicated by common risk variants identified in genome-wide association studies (GWAS) and by rare variants in sequencing studies of rare ED syndromes that co-present with HS. EDs are Mendelian (i.e., single-gene) disorders that disrupt the development of ectodermal derivatives, including hair follicles and sweat glands. The enrichment of ED-associated genes in HS genetic studies, together with HS phenotypes observed in ED patients, supports a critical role for aberrant follicular development in HS pathogenesis. We propose that HS represents a spectrum of related diseases entities spanning immune dysregulation and hair follicle pathology, underscoring the need for biomarkers and refined disease classification to tailor treatment strategies. This perspective argues for broadening drug-development programs and insurance coverage for therapeutic strategies beyond immunomodulation to include follicle-targeted approaches.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 7","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70321","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148411133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Site-Specific Immunological Changes Induced by Narrowband UVB in Acral and Non-Acral Vitiligo","authors":"Keshavamurthy Vinay,&nbsp;Hitaishi Mehta,&nbsp;Anish Thind,&nbsp;Hitaishi Kaushik,&nbsp;Muthu Sendhil Kumaran,&nbsp;Davinder Parsad,&nbsp;Vinod Kumar","doi":"10.1111/exd.70325","DOIUrl":"10.1111/exd.70325","url":null,"abstract":"<div>\u0000 \u0000 <p>Acral vitiligo responds less well to NB-UVB than non-acral disease, but site-specific immunologic changes during therapy are incompletely defined. The objective of this study was to compare NB-UVB–associated changes in T cell subsets and soluble mediators in acral versus non-acral vitiligo. Thirty patients with non-segmental vitiligo were enrolled. Ten underwent paired biopsies (acral and non-acral) before and after 6 months of NB-UVB for flow cytometry (Tregs, CD8+ T cells, CD8+CD45RO+ memory T cells, CD8+CD69+CD103+ TRM). Suction-blister fluid ELISA assessed IFN-γ–axis mediators (CXCR3, CXCL9, CXCL10, IFN-<i>γ</i>, IL-1β) in two separate groups: 10 treatment-naïve patients and 10 patients who had completed 6 months of NB-UVB therapy. Non-parametric tests used Benjamini–Hochberg FDR correction (pFDR). In paired biopsies (<i>n</i> = 10; CD8 <i>n</i> = 9), memory T cells decreased after NB-UVB in acral (4.38 [3.47–5.98] to 1.38 [0.73–2.21]; pFDR = 0.041) and non-acral lesions (5.23 [4.27–6.75] to 1.08 [0.48–2.54]; pFDR = 0.0039). TRM declined in acral (5.95 [3.17–7.41] to 0.65 [0.15–1.15]; pFDR = 0.0039) and non-acral sites (4.12 [2.50–5.57] to 0.69 [0.28–1.19]; pFDR = 0.0039). Tregs showed a site-divergent pattern: acral Tregs decreased (0.56 [0.41–0.75] to 0.08 [0.03–0.23]; pFDR = 0.0067) while non-acral Tregs increased (0.40 [0.24–0.61] to 0.95 [0.41–1.59]; pFDR = 0.0039). CD8+ T cells showed no change after correction. CXCL9 showed a non-significant decreasing trend (pFDR = 0.249); no ELISA marker remained significant after FDR correction. NB-UVB exerts a pronounced effect on cellular immunity (reductions in TRM and memory T cells) with limited cytokine suppression, with site-divergent Treg pattern.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 7","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148404165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}