Experimental Dermatology最新文献_第6页

Fibroblast State Remodelling and Stromal Depletion Shape the Ageing Microenvironment of Human Penile Skin 成纤维细胞状态重塑和基质耗竭塑造了人类阴茎皮肤老化微环境。

IF 3.4 3区医学

Experimental Dermatology Pub Date : 2026-07-07 DOI: 10.1111/exd.70322

Yu Yang, Honghao Yu, Pingping Lin, Hang Li, Binbin Lai

{"title":"Fibroblast State Remodelling and Stromal Depletion Shape the Ageing Microenvironment of Human Penile Skin","authors":"Yu Yang, Honghao Yu, Pingping Lin, Hang Li, Binbin Lai","doi":"10.1111/exd.70322","DOIUrl":"10.1111/exd.70322","url":null,"abstract":"<div>\u0000 \u0000 Disentangling intrinsic (chronological) skin ageing from ultraviolet-driven photoaging remains challenging because most human skin single-cell studies are biassed towards sun-exposed sites and non-genital anatomy. Here, we profiled histologically normal human penile skin, a typically UV-shielded mucocutaneous niche, to characterise ageing-associated remodelling in a specialised cutaneous microenvironment. We analysed 137 880 cells from 13 healthy male donors (13–63 years) and identified 12 major cell types. Donor-aware compositional profiling revealed pronounced age-associated stromal depletion, driven by progressive loss of fibroblasts and pericyte/vascular smooth muscle cells. Whole-skin pseudo-bulk modelling across continuous age captured broad transcriptional drift towards senescence- and inflammation-related programmes alongside reduced extracellular matrix organisation and Wnt-associated maintenance pathways. Cell type-resolved pseudo-bulk analyses localised the strongest age-associated changes to stromal lineages. In fibroblasts, unsupervised temporal module analysis indicated a shift from matrix-supportive/regenerative programmes towards a pro-inflammatory, senescence-associated secretory phenotype-like state. Cross-compartment overlap further identified a 21-gene core module shared across epidermal, stromal, and immune compartments in older donors, consistent with coordinated tissue-wide remodelling. Together, these findings nominate stromal attrition and inflammatory fibroblast reprogramming as central features of ageing in human penile skin and provide a site-specific framework for distinguishing conserved intrinsic ageing modules from niche-shaped execution mechanisms. This UV-shielded genital reference offers a complementary baseline for interpreting intrinsic ageing signals across anatomically diverse skin sites.\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":"148404107","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}

引用次数: 0

Beyond Lymphocytes: HCA2 Receptor Signalling Tunes the Skin-Resident Threshold for Contact Allergy 超越淋巴细胞：HCA2受体信号调节皮肤接触性过敏阈值。

IF 3.4 3区医学

Experimental Dermatology Pub Date : 2026-07-06 DOI: 10.1111/exd.70316

Youngae Lee, Dong Hun Lee

引用次数: 0

SLURP2 Enlarges Adipocytes and Induces IL-23-Producing Macrophages in Murine Dermal Adipose Tissue SLURP2在小鼠真皮脂肪组织中增加脂肪细胞并诱导产生il -23的巨噬细胞。

IF 3.4 3区医学

Experimental Dermatology Pub Date : 2026-07-06 DOI: 10.1111/exd.70304

Hitomi Tsuji, Tomotaka Mabuchi

{"title":"SLURP2 Enlarges Adipocytes and Induces IL-23-Producing Macrophages in Murine Dermal Adipose Tissue","authors":"Hitomi Tsuji, Tomotaka Mabuchi","doi":"10.1111/exd.70304","DOIUrl":"10.1111/exd.70304","url":null,"abstract":"Dermal adipocytes have unique features different from visceral and subcutaneous adipocytes. Their cyclic remodelling is coupled with hair follicle (HF) cycling: expansion in the anagen and reduction in the catagen stages. Secreted Ly6/uPAR related protein 2 (SLURP2) is a non-neuronal transmitter and a ligand of both nicotinic and muscarinic acetylcholine receptors. It is upregulated in psoriatic lesions. Mouse SLURP2-deficient mice exhibit reduced adiposity and plasma cholesterol levels, in addition to palmoplantar keratoderma. However, the effects of SLURP2 on adipocytes remain unexplored. Here, we demonstrated that SLURP2 regulates murine dermal adipocyte size independently of HF cycling and upregulates interleukin (IL)-23 gene expression following intradermal injection of recombinant human SLURP2-Fc protein (rSLURP2) and phosphate-buffered saline (control) at different dorsal sites of C57BL/6J mice after depilation. SLURP2 enlarged dermal adipocytes independently of HF cycles by inhibiting sterol regulatory element-binding protein-1, a transcription factor involved in cholesterol and fatty acid synthesis, which leads to the activation of cholesterol synthesis followed by expansion of the plasma and lipid droplet membrane. Immunohistochemical staining of paired mirror sections revealed a statistically significant increase in the ratio of IL-23-producing macrophages in the dermal adipose tissue of rSLURP2-injected skin compared with the control. Furthermore, IL-23p19 gene expression was significantly upregulated in rSLURP2-treated skin. Taken together with the previous findings, the present study showed that SLURP2 has inflammatory and metabolic effects. Dermal adipose tissues may serve as a source of IL-23 in psoriatic lesions.","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 7","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70304","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390236","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}

引用次数: 0

Type I and II Interferon Signalling Characterizes the Transcriptional Landscape of Sweet Syndrome I型和II型干扰素信号传导表征甜综合征的转录景观。

IF 3.4 3区医学

Experimental Dermatology Pub Date : 2026-07-06 DOI: 10.1111/exd.70323

Laura Calabrese, Chiara Moltrasio, Maurizio Romagnuolo, Pia-Charlotte Stadler, Zeno Fiocco, Matthias Neulinger-Muñoz, Rui Aoki, Martina D'Onghia, Pietro Rubegni, Katrin Kerl, Takashi K. Satoh, Angelo V. Marzano, Lars E. French

{"title":"Type I and II Interferon Signalling Characterizes the Transcriptional Landscape of Sweet Syndrome","authors":"Laura Calabrese, Chiara Moltrasio, Maurizio Romagnuolo, Pia-Charlotte Stadler, Zeno Fiocco, Matthias Neulinger-Muñoz, Rui Aoki, Martina D'Onghia, Pietro Rubegni, Katrin Kerl, Takashi K. Satoh, Angelo V. Marzano, Lars E. French","doi":"10.1111/exd.70323","DOIUrl":"10.1111/exd.70323","url":null,"abstract":"Sweet syndrome (SS) is an autoinflammatory neutrophilic dermatosis characterized by abrupt-onset inflammatory skin lesions and systemic symptoms, yet its molecular pathogenesis remains incompletely defined. To delineate disease-specific inflammatory programmes, we performed NanoString-based transcriptomic analysis of SS skin lesions and compared them with healthy control skin and pyoderma gangrenosum, a related neutrophilic dermatosis. SS exhibited a distinct inflammatory transcriptional signature marked by robust upregulation of type I and II interferon–stimulated genes, including CXCL9, CXCL10, GBP1, GBP5, IFIT2 and IRF7, distinguishing SS from both control groups. Cell type deconvolution analysis revealed enrichment of dendritic cells, consistent with a prominent type I interferon-driven immune response. In parallel, SS lesions demonstrated altered immunoproteasome gene expression, with upregulation of immunoproteasome subunits PSMB8, PSMB9 and PSMB10 and downregulation of the constitutive subunit PSMB7 suggesting functional remodelling of proteasomal activity. Together, these findings support a model in which dendritic cell-driven interferon signalling promotes immunoproteasome remodelling and sustains neutrophilic inflammation in Sweet. This study identifies a prominent interferon signalling as a defining molecular feature of SS and highlights potential therapeutic opportunities within the interferon–JAK/STAT and proteasome pathways.","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 7","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70323","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148396596","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}

引用次数: 0

Comparative Transcriptomics Reveals SKH-1 Mice as a Valuable Model for Psoriasis Pathogenesis and Recurrence Studies 比较转录组学揭示SKH-1小鼠是银屑病发病机制和复发研究的有价值模型。

IF 3.4 3区医学

Experimental Dermatology Pub Date : 2026-07-05 DOI: 10.1111/exd.70324

Lixin Yue, Yaxing Bai, Bingyu Pang, Pei Qiao, Ke Xue, Lizhi Hu, Gang Wang, Erle Dang

{"title":"Comparative Transcriptomics Reveals SKH-1 Mice as a Valuable Model for Psoriasis Pathogenesis and Recurrence Studies","authors":"Lixin Yue, Yaxing Bai, Bingyu Pang, Pei Qiao, Ke Xue, Lizhi Hu, Gang Wang, Erle Dang","doi":"10.1111/exd.70324","DOIUrl":"10.1111/exd.70324","url":null,"abstract":"<div>\u0000 \u0000 Psoriasis is a complex chronic inflammatory and autoimmune disease; therefore, reliable and human-relevant animal models are essential for preclinical drug testing and mechanistic studies. SKH-1 mice, which lack functional hair follicles and display a thickened epidermis that more closely resembles human skin than that of C57BL/6 mice, represent a potential psoriasis model, but their suitability remains uncertain. In this study, proliferation, barrier function, differentiation, and inflammatory responses were assessed in the imiquimod (IMQ)-induced dermatitis model of SKH-1 mice using qRT-PCR, immunofluorescence, and flow cytometry. Transcriptomic profiling via RNA sequencing was performed on total RNA from lesional and non-lesional skin of IMQ-induced SKH-1 mice, IMQ-induced C57BL/6 mice, and human psoriatic skin. A psoriasis-like mouse model was also established in SKH-1 mice to evaluate its utility for recurrence studies. The results showed that the IMQ-induced SKH-1 mouse model exhibited hyperproliferation, hypodifferentiation, barrier disruption, and excessive inflammatory responses similar to human psoriasis. Transcriptomic analysis further highlighted the advantages and complementarity of this model in studying psoriasis pathogenesis, and the established recurrence model provided a suitable tool for investigating the mechanisms of psoriasis recurrence. This study compared the transcriptomic signatures of lesional skin between IMQ-induced SKH-1 and C57BL/6 mice and demonstrated that the SKH-1 model can recapitulate vascular dysregulation and disease recurrence, indicating that it serves as a valuable complementary tool for probing psoriasis pathogenesis.\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 7","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390157","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}

引用次数: 0

M2 Macrophage–Derived ENPP2/LPA Signalling Attenuates UVB-Induced Fibroblast Photoaging via LPAR1/3 M2巨噬细胞来源的ENPP2/LPA信号通过LPAR1/3减弱uvb诱导的成纤维细胞光老化。

IF 3.4 3区医学

Experimental Dermatology Pub Date : 2026-07-02 DOI: 10.1111/exd.70313

Meiqi Lu, Xiaoyang Wang, Yujie Hu, Shanshan Jia, Yongjun Qi, Ya Jiao, Jie Zhao, Xiaochuan Wang, Jixun Zhang, Duyin Jiang

{"title":"M2 Macrophage–Derived ENPP2/LPA Signalling Attenuates UVB-Induced Fibroblast Photoaging via LPAR1/3","authors":"Meiqi Lu, Xiaoyang Wang, Yujie Hu, Shanshan Jia, Yongjun Qi, Ya Jiao, Jie Zhao, Xiaochuan Wang, Jixun Zhang, Duyin Jiang","doi":"10.1111/exd.70313","DOIUrl":"10.1111/exd.70313","url":null,"abstract":"<div>\u0000 \u0000 Chronic exposure to ultraviolet B (UVB) radiation induces excessive reactive oxygen species (ROS) production in dermal fibroblasts, leading to cellular senescence and skin photoaging. Ageing skin is characterised by disruption of the immune microenvironment, including impaired macrophage polarisation and reduced M2 macrophage activity. However, the contribution of M2 macrophages to fibroblast photoaging remains incompletely understood. Here, we investigated whether M2 macrophages attenuate UVB-induced fibroblast senescence through ectonucleotide pyrophosphatase/phosphodiesterase 2 (ENPP2)–dependent lysophosphatidic acid (LPA)signalling. UVB-induced L929 fibroblasts were treated with conditioned media derived from polarised RAW264.7 macrophages, with or without ENPP2 silencing. UVB exposure induced marked senescence, oxidative stress, and mitophagy impairment, whereas conditioned medium from M2 macrophages significantly alleviated these effects compared with M1-derived conditioned medium. Notably, ENPP2 depletion in M2 macrophages substantially reduced these protective effects. M2 macrophage–derived conditioned medium contained elevated LPA levels and restored UVB-suppressed LPAR1 and LPAR3 expression in fibroblasts. Pharmacological inhibition of LPAR1/3 attenuated the protective effects of M2 macrophages, while exogenous LPA supplementation restored these effects under ENPP2-deficient conditions. These changes were associated with enhanced PINK1/Parkin-related mitophagy signalling and reduced oxidative stress. Collectively, these findings identify M2 macrophage–derived ENPP2/LPA signalling as a critical paracrine mechanism that mitigates UVB-induced fibroblast photoaging.\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 7","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148374964","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}

引用次数: 0

Human-Relevant In Vitro Skin Models: From Regulatory-Validated Platforms to Emerging Technologies for Translational Dermatology 人类相关的体外皮肤模型：从监管验证的平台到转化皮肤病学的新兴技术。

IF 3.4 3区医学

Experimental Dermatology Pub Date : 2026-07-02 DOI: 10.1111/exd.70312

So Young Lee, Soeun Jeon, Kui Young Park, Ji Yeon Hong

{"title":"Human-Relevant In Vitro Skin Models: From Regulatory-Validated Platforms to Emerging Technologies for Translational Dermatology","authors":"So Young Lee, Soeun Jeon, Kui Young Park, Ji Yeon Hong","doi":"10.1111/exd.70312","DOIUrl":"10.1111/exd.70312","url":null,"abstract":"The rapid advancement of human-relevant in vitro skin models has been driven by increasingly stringent regulatory restrictions on animal testing and the growing recognition that conventional animal and two-dimensional cell culture systems fail to accurately predict human skin biology and clinical outcomes. Three-dimensional reconstructed human skin models, ex vivo human skin platforms, and next-generation bioengineered systems have been recognized as critical tools for dermatological research, cosmetic safety assessment, and pharmaceutical development. This review focuses on commercially available in vitro human skin models currently used in regulatory and research settings, as well as emerging technologies under active development. We provide an overview of reconstructed human epidermis and full-thickness skin equivalents, functional variants incorporating pigmentation and microbiome support, and ex vivo human skin models derived from surgical tissues. Additionally, we discuss cutting-edge platforms, including vascularized and perfused skin models, immune-competent skin constructs, organoid-based appendage-containing models, and microbiome-integrated platforms. Furthermore, we highlight current limitations, regulatory gaps, and future directions for standardization, scalability, and clinical translation. Collectively, advanced human skin models are expected to significantly enhance dermatological research by enabling predictive, ethical, and mechanistically informative testing strategies that bridge the gap between in vitro experimentation and clinical outcomes.","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 7","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70312","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148367653","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}

引用次数: 0

Deep Phenotyping and Molecular Elucidation of a New Syndrome: Ectodermal Dysplasia Caused by IRF6 Variants. 一种新的综合征：由IRF6变异引起的外胚层发育不良的深层表型和分子解析。

IF 3.4 3区医学

Experimental Dermatology Pub Date : 2026-07-01 DOI: 10.1111/exd.70331

Holm Schneider, Smail Hadj-Rabia, Carola Berking, Matthias Weider, Julie Steffann, Ralf J Rieker, Lina Gölz, Nicolai Peschel

{"title":"Deep Phenotyping and Molecular Elucidation of a New Syndrome: Ectodermal Dysplasia Caused by IRF6 Variants.","authors":"Holm Schneider, Smail Hadj-Rabia, Carola Berking, Matthias Weider, Julie Steffann, Ralf J Rieker, Lina Gölz, Nicolai Peschel","doi":"10.1111/exd.70331","DOIUrl":"10.1111/exd.70331","url":null,"abstract":"The diagnosis of an ectodermal dysplasia (ED) is often made by dermatologists. Some of the more than 50 distinct ectodermal dysplasias, however, are still largely unknown and their pathogenesis is poorly understood. Since we recently discovered that variants of the Interferon Regulatory Factor 6 (IRF6) gene IRF6 may cause ED, we have further investigated the link between this gene and maldevelopment of tissues originating from the embryonic ectoderm. Disease characterization in two previously reported subjects and one newly identified patient (mosaic status) included systematic clinical and genetic evaluation, assessment of all available patient records and dental radiographs, hearing tests and immunostaining of skin samples. Structural models of native and mutant IRF6 were analysed to elucidate the pathogenesis. IRF6-associated ED, a combination of natal teeth (irregularly), absent sweat glands, hidradenitis suppurativa-like symptoms, onychodysplasia, agenesis of numerous deciduous and permanent teeth, and sensorineural hearing impairment, was linked to amino acid substitutions in a region between the DNA-binding domain and the protein-binding domain of IRF6, which has not yet been assigned a function. Genotype-phenotype correlations from a total of five patients and immunohistochemical data support the assumption that IRF6-associated ED is based on a gain-of-function mechanism. Thus, IRF6 variants are not only the cause of Van der Woude syndrome and popliteal pterygium syndrome, two diseases with cleft lip/palate as common features, but are most likely responsible also for a new, challenging syndrome without orofacial clefting. Our results facilitate accurate and early diagnosis in affected individuals and may pave the way for specific treatment.","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 7","pages":"e70331"},"PeriodicalIF":3.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13392586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148561311","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}

引用次数: 0

Revisiting Type VII Collagen Mislocalisation in Dystrophic Epidermolysis Bullosa Using High-Resolution Imaging. 利用高分辨率成像重新审视营养不良大疱性表皮松解症中VII型胶原蛋白的错误定位。

IF 3.4 3区医学

Experimental Dermatology Pub Date : 2026-07-01 DOI: 10.1111/exd.70330

Mika Watanabe, Kazuki Watanabe, Satoru Shinkuma, Hideyuki Ujiie, Ken Natsuga

{"title":"Revisiting Type VII Collagen Mislocalisation in Dystrophic Epidermolysis Bullosa Using High-Resolution Imaging.","authors":"Mika Watanabe, Kazuki Watanabe, Satoru Shinkuma, Hideyuki Ujiie, Ken Natsuga","doi":"10.1111/exd.70330","DOIUrl":"10.1111/exd.70330","url":null,"abstract":"Type VII collagen (COL7), a major component of anchoring fibrils, is essential for dermal-epidermal adhesion and pathogenic variants in COL7A1, encoding COL7, cause dystrophic epidermolysis bullosa (DEB). In normal skin, COL7 is localised just beneath the lamina densa. In contrast, previous immunoelectron microscopy (IEM) studies of DEB skin with residual COL7 expression demonstrated aberrant localisation of COL7 above the lamina densa and hemidesmosomes of epidermal basal keratinocytes, possibly reflecting impaired secretion of defective COL7. However, conventional microscopy techniques lack sufficient spatial resolution to clearly visualise individual protein distributions and resolve this finding. Here, we revisit the abnormal localisation of COL7 using two higher-resolution approaches: structured illumination microscopy (SIM) and expansion microscopy (ExM). In normal human skin, the COL7 NC1 domain colocalised with type IV collagen (COL4), a surrogate marker of the lamina densa and was consistently detected beneath integrin α6 (ITGA6), a hemidesmosomal marker. In DEB skin with residual COL7 expression, COL7 was detected above ITGA6 within basal keratinocytes, recapitulating previous IEM observations. SIM quantitatively confirmed significant BMZ disorganisation in DEB, whereas ExM showed a consistent but non-significant trend, likely due to variability in expansion factors. These findings demonstrate that high-resolution fluorescence imaging can reproduce classic IEM observations of COL7 mislocalisation, suggesting its potential as a more accessible complementary approach for morphologic assessment of DEB.","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 7","pages":"e70330"},"PeriodicalIF":3.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13379322/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148469849","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}

引用次数: 0

Clinical Significance of Malassezia-Specific IgE in Assessing the Severity of Head and Neck Involvement in Korean Atopic Dermatitis Patients. 马拉色菌特异性IgE在评估韩国特应性皮炎患者头颈部受累程度中的临床意义。

IF 3.4 3区医学

Experimental Dermatology Pub Date : 2026-07-01 DOI: 10.1111/exd.70334

Han-Na Kim, Jaewon Choi, Anna Kim, Ko Eun Kim, Yoo Sang Baek, Jiehyun Jeon

{"title":"Clinical Significance of Malassezia-Specific IgE in Assessing the Severity of Head and Neck Involvement in Korean Atopic Dermatitis Patients.","authors":"Han-Na Kim, Jaewon Choi, Anna Kim, Ko Eun Kim, Yoo Sang Baek, Jiehyun Jeon","doi":"10.1111/exd.70334","DOIUrl":"10.1111/exd.70334","url":null,"abstract":"Head and neck dermatitis (HND) is a distinct clinical phenotype of atopic dermatitis (AD). While Malassezia sensitisation and elevated Malassezia-specific IgE antibody (MSIA) levels have been documented in HND patients, the relationship between MSIA levels and disease severity remains controversial. The primary aim of our study was to evaluate whether MSIA levels correlate with the severity of HND. This retrospective observational study was conducted at a single tertiary center and included 121 patients with AD. Laboratory data included serum MSIA, house dust mite (HDM)-specific IgE and total IgE levels. Clinical severity was measured using the global Eczema Area and Severity Index (EASI) and partial HND EASI scores. We introduced a novel metric, the 'relative HND severity score', defined as the HND EASI score divided by the global EASI score. Spearman's Rho correlation analyses were used to examine the correlations between different IgE levels and severity scores. The HND EASI score demonstrated significant positive correlations with MSIA (r = 0.569, p < 0.001) and both HDM-specific antibodies: D1 (r = 0.247, p = 0.007) and D2 (r = 0.267, p = 0.004). The relative HND severity score was significantly positively correlated with MSIA (r = 0.353, p < 0.001), but not with HDM-specific antibodies (D1, p = 0.985; D2, p = 0.974). Age-stratified subgroup analyses revealed significant positive correlations between MSIA and both absolute (r = 0.591, p < 0.001) and relative HND severity (r = 0.344, p = 0.002) only in the adult cohort. In conclusion, serum MSIA levels significantly correlate with the clinical severity of HND in Korean AD patients. This association is most clearly observed in the adult population.","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 7","pages":"e70334"},"PeriodicalIF":3.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13400888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148583927","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}

引用次数: 0