Experimental Dermatology最新文献

{"title":"Basal Cell Carcinoma May Be Associated With Staphylococcus Dysbiosis","authors":"Justin G. Schlager,&nbsp;Daniel Stiefel,&nbsp;Kathrin Patzer,&nbsp;Michael Schloter,&nbsp;Bärbel U. Foesel,&nbsp;Nathalie M. Zelzer,&nbsp;Lars E. French,&nbsp;Silvia Gschwendtner,&nbsp;Daniela Hartmann","doi":"10.1111/exd.70371","DOIUrl":"https://doi.org/10.1111/exd.70371","url":null,"abstract":"<div>\u0000 \u0000 <p>There is growing evidence that a dysbiosis of the skin microbiome has an impact on carcinogenesis in cutaneous squamous cell carcinoma. However, the role of the microbiome in basal cell carcinoma (BCC) remains unclear due to limited, inconsistent, ex vivo studies. Here, we analysed the skin microbiome of patients with BCC, including the tumour lesion as well as perilesional skin from the same subject. Skin swabs from BCC and perilesional skin were taken prior to tumour surgery. After DNA extraction, we used a metabarcoding approach based on 16S rRNA gene amplicon sequencing to analyse the cutaneous bacterial communities. In total, 63 patients with BCC were included for analysis. Most tumour lesions were located on sun-exposed, sebaceous areas such as the nose, cheeks, and forehead. The genera <i>Corynebacterium, Cutibacterium</i>, and <i>Staphylococcus</i> predominated both in BCC and perilesional skin. However, the microbiome of BCC was reduced in overall bacterial richness, with a significant overabundance of amplicon sequence variants (ASV) assigned to the genus <i>Staphylococcus</i>, resulting in a reduced complexity in microbial networks. The dominating ASV assigned to <i>Staphylococcus</i> was also detected in perilesional skin regions, indicating that the microbial dysbiosis in BCC affected regions is caused by natural members of the healthy skin microbiome. The BCC microbiome is characterised by microbial dysbiosis, reflected by a reduced overall bacterial richness, fewer microbe-microbe interactions and a significant over-representation of <i>Staphylococcus</i> species compared with perilesional skin. Further long-read metagenomics and cultivation-based studies are needed to identify <i>Staphylococcus</i> species driving dysbiosis.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 10","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149205970","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":"Spatial and Single-Cell Multi-Omics Analyses of T-Cell Subsets and Interactions in Melanoma Lymph Node Metastasis","authors":"Ras Azira Ramli,&nbsp;Samuel Tan,&nbsp;Yibi Chen,&nbsp;Glen Boyle,&nbsp;Quan Nguyen","doi":"10.1111/exd.70376","DOIUrl":"10.1111/exd.70376","url":null,"abstract":"<p>Melanoma is a highly immunogenic malignancy, yet responses to systemic therapy remain variable. The tumour-draining lymph node (TDLN), including the sentinel lymph node (SLN) during early regional spread, is not only a site of metastatic dissemination but also an important setting for T-cell priming and immune regulation. Conventional classification of nodes as tumour-positive or tumour-negative provides essential staging information but reveals little about their immune state. Single-cell immune transcriptomics, T-cell receptor sequencing and single-cell epigenomics now allow T-cell states, clonal dynamics and regulatory programmes to be examined in greater detail. Spatial transcriptomics, multiplex imaging, spatial proteomics and emerging spatial metabolomics add the anatomical context needed to determine where these cells and molecular programmes occur within the intact tissue architecture. In this review, we examine how these approaches are being utilised to study T-cell heterogeneity, spatial organisation and immune interactions within melanoma TDLNs, together with the emerging contribution of artificial intelligence (AI)-assisted pathology. We also critically evaluate how these technologies are applied, with attention to tissue requirements, spatial resolution, molecular coverage, computational demands, scalability to archival haematoxylin and eosin (H&amp;E) imaging cohorts and careful interpretation of predicted or inferred spatial features. By combining biological profiling with methodological appraisal, we highlight how multi-omics immune signatures may refine nodal disease assessment and guide future biomarker development, while noting that clinical translation will require standardised analytical pipelines and disease-specific validation across independent melanoma cohorts.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 10","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70376","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180182","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":"Plant-Derived Senolytic Ingredient, Camellia sinensis Root Extract, Ameliorates Skin Aging-Associated Phenotypes","authors":"Sunyoung Park,&nbsp;Siyoung Cho,&nbsp;Daejin Min,&nbsp;Hyunjung Choi,&nbsp;Kyeonghwan Hwang,&nbsp;In Sup Kil,&nbsp;Won-Seok Park,&nbsp;Hyoung-June Kim","doi":"10.1111/exd.70366","DOIUrl":"10.1111/exd.70366","url":null,"abstract":"<p>Senescent cells affect neighbouring cells via the senescence-associated secretory phenotype (SASP), which involves proinflammatory cytokines, chemokines and proteases. <i>Camellia sinensis</i> root extract (SENOMUNE) has shown therapeutic potential for skin aging-related disorders. However, whether it exerts senolytic effect remains to be explored. Thus, this study aimed to assess the senolytic properties of SENOMUNE in a stress-induced premature senescence model in normal human dermal fibroblasts (NHDFs) through cell viability assays, quantitative reverse transcription polymerase chain reaction, western blot and flow cytometry. NHDFs were induced to senescence using doxorubicin and insulin-like growth factor-1. The senolytic effect of SENOMUNE was evaluated by measuring senescence-associated β-galactosidase activity, gene and protein expression, and the apoptosis rate. SENOMUNE reduced the viability of senescent cells in a dose-dependent manner, with a more pronounced effect in senescent cells than in control cells. It was also associated with caspase-independent programmed cell death involving apoptosis-inducing factor and lysosomal membrane permeabilization in senescent cells. Moreover, SENOMUNE reduced the production of SASP factors, increased the expression of skin barrier-associated markers, and attenuated pigmentation by modulating the secretion of inflammatory cytokines. These effects were evaluated using conditioned media derived from senescent fibroblasts and validated through ex vivo skin biopsy experiments. Our results suggest that SENOMUNE exhibits senolytic properties and thus is a promising anti-aging phytopharmaceutical ingredient for managing skin-related disorders.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 10","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13659427/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149172225","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":"Vitamin D3 Inhibits Expression of Interleukin-6 and Calcitonin Gene-Related Peptide by Transformed Dorsal Root Ganglion Neurons","authors":"Jiong Zhou,&nbsp;Wanhong Ding,&nbsp;Lori L. Stohl,&nbsp;Katherine Alerte,&nbsp;Xi K. Zhou,&nbsp;Sarah A. Commaroto,&nbsp;Sharan Grover,&nbsp;Almayasa Al-Marri,&nbsp;Michelle Lee,&nbsp;Richard D. Granstein","doi":"10.1111/exd.70374","DOIUrl":"10.1111/exd.70374","url":null,"abstract":"<div>\u0000 \u0000 <p>Interleukin-6 (IL-6) and the neuropeptide calcitonin gene-related peptide (CGRP) promote the generation of T helper 17 (Th17) cells. Th17-type immunity is involved in several autoimmune disorders, including psoriasis. Also, there is evidence that sensory nerves play a role in Th17-type immunity, including in psoriasis. Vitamin D (VD) blood levels vary inversely with the severity of psoriasis, and topical VD analogs are effective treatments for this disease. We have now asked whether 25-dihydroxyvitamin D3 [25(OH)D₃] and the more potent, active analog 1α,25-dihydroxyvitamin D3 [1α,25(OH)₂D₃] inhibit IL-6 and/or α-CGRP production by transformed mouse embryonic dorsal root ganglion (DRG) neurons (MED17.11 cells), which serve as a surrogate for primary DRG neurons. After culture in differentiation medium, MED17.11 cells express markers of mature DRG neurons. Lymph nodes are innervated, so IL-6 and CGRP released from nerves are anatomically situated to influence Th17 cell generation. MED17.11 cells were cultured in differentiation medium for 48-h to induce differentiation; then, medium in each well was replaced with fresh differentiation medium containing a range of concentrations of 25(OH)D₃ or 1α,25(OH)₂D₃. Twenty-four and 48-h later, supernatants were collected, and cells were harvested and lysed. IL-6 and α-CGRP content of supernatants and lysates were assessed by ELISA. Both 25(OH)D₃ and 1α,25(OH)₂D₃ significantly inhibited IL-6 content of supernatants and α-CGRP content of cell lysates in a dose-dependent manner with 1α,25(OH)₂D₃ being more potent. 25(OH)D₃ and 1α,25(OH)₂D₃ also inhibited expression of IL-6 mRNA. VD may beneficially affect disorders involving Th17-type immunity by decreasing expression of IL-6 and α-CGRP by DRG nerves.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 10","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149165009","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":"ECM1 Loss in Oral Keratinocytes Impairs Proliferation and Migration While Promoting Keratinization and EMT-Like Remodelling: A Cell-Based Model for the Oral Manifestations of Lipoid Proteinosis","authors":"Suxuan Xu,&nbsp;Qiyu Chen,&nbsp;Tong Zhao,&nbsp;Sijing Xie,&nbsp;Wenlei Wu,&nbsp;Jie Yang,&nbsp;Juan Wu","doi":"10.1111/exd.70373","DOIUrl":"10.1111/exd.70373","url":null,"abstract":"<div>\u0000 \u0000 <p>Lipoid proteinosis (LP) is a rare autosomal recessive disorder caused by loss-of-function mutations in the extracellular matrix protein 1 (ECM1) gene. While the clinical features of LP are well documented, the cellular mechanisms underlying its oral manifestations, particularly the direct consequences of ECM1 deficiency in oral keratinocytes, remain poorly understood. This study investigated the role of ECM1 in human oral keratinocytes (HOK) using an in vitro gain- and loss-of-function model. Functional assays were performed to evaluate proliferation, migration, keratinization and epithelial-mesenchymal transition (EMT)-like remodelling, complemented by transcriptomic sequencing (RNA-seq) to profile global transcriptional changes. ECM1 knockdown inhibited HOK proliferation and migration, while concomitantly promoting keratinization and an EMT-like remodelling response. Protein-level analyses confirmed activation of the TGF-β/Smad signalling pathway, with elevated p-Smad2/3 and increased secretion of TGF-β1 and MMP-9. RNA-seq analysis identified perturbations in genes and pathways governing cell cycle, motility and differentiation. Immunohistochemical validation in LP patient tissue showed COL4A1 deposition matching the characteristic PAS-positive hyaline material. Loss of ECM1 function may contribute to oral LP features through a dual mechanism: impairing tissue repair by hampering keratinocyte proliferation and migration, and promoting tissue remodelling through aberrant keratinization and an EMT-like phenotypic shift. These findings offer a cell-based model for understanding the oral manifestations of LP and highlight the epithelial contribution to LP-associated tissue remodelling.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 10","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135076","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":"Melanosome Clusters and Apoptotic Melanocytes Internalized by Dermal Fibroblasts Impairs Cellular Function","authors":"Yangyi Jin,&nbsp;Zhe Feng,&nbsp;Xingge Huang,&nbsp;Ruonan Qian,&nbsp;Muyang Shi,&nbsp;Lingling Xuan,&nbsp;Yaling Song,&nbsp;Xiao Feng,&nbsp;Hu Huang,&nbsp;Jing Wang,&nbsp;Hideya Ando","doi":"10.1111/exd.70302","DOIUrl":"10.1111/exd.70302","url":null,"abstract":"<div>\u0000 \u0000 <p>Skin pigmentation disorders with dermal melanin involvement are therapeutically challenging due to poor responsiveness to conventional treatments and unclear pathogenesis. While melanin in the dermis is typically cleared by macrophages, human dermal fibroblasts (HDFs) can also internalize extracellular melanosome clusters (EMC) and apoptotic melanocytes that have occasionally been observed in the dermis, which may contribute to persistent pigment-related abnormalities. However, the functional impact of phagocytosis for fibroblasts remains unclear. In this study, HDFs were incubated with EMC or apoptotic MNT-1 melanoma cells (ApoMNT-1)—both exposing the phagocytic “eat-me” signal phosphatidylserine—confirming their internalization via Annexin V and TEM assays. Phagocytosis of EMC and ApoMNT-1 significantly upregulated the mRNA expression of IL-6, IL-8, IL-1β, PTGS2, and NF-κB, as well as the protein levels. Additionally, HDF proliferation was markedly inhibited, and the mRNA and protein levels of COL-1 and COL-3 were reduced. Furthermore, HDF mitochondrial function was impaired by the phagocytosis of EMC or ApoMNT-1, as indicated by decreases in basal respiration, ATP production, glycolysis, glycolytic capacity, and mitochondrial membrane potential. These results suggest that HDF internalization of EMC and apoptotic melanocytes triggers pro-inflammatory responses, inhibits cell proliferation and collagen synthesis, and impairs mitochondrial function. These findings provide novel insights into the biological mechanisms of dermal melanin-related processes and the functional changes of dermal fibroblasts after melanin phagocytosis, which lays a foundation for further in vivo studies on dermal hyperpigmentation.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 10","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149106479","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":"The Spatiotemporal Coupling Imbalance of Senescent Grey Hair: Remodelling of the HFSC–MeSC–Niche Network and a New Paradigm of Stem Cell Senescence","authors":"Hanyu Xu,&nbsp;Xiuzu Song","doi":"10.1111/exd.70365","DOIUrl":"10.1111/exd.70365","url":null,"abstract":"<p>This review examines age-related hair greying as a potential imbalance in the HFSC–MeSC–niche network in terms of time, space and signal quality. We define signal quality as the effective strength, temporal precision and noise-to-threshold relationship of niche-derived cues that regulate MeSC activation. We propose that ageing may progressively weaken the temporal coordination between HFSC activation and MeSC responsiveness. ECM remodelling and altered guidance-related cues may further impair MeSC niche engagement. Meanwhile, chronic oxidative stress, low-grade inflammation and stress-related sympathetic norepinephrine signalling may increase background noise, distort signal timing and push the MeSC activation threshold upward, so residual MeSC-lineage cells may fail to engage effectively with the niche. Such functional uncoupling may represent an early or intermediate stage, whereas sustained genotoxic stress or niche failure can eventually drive irreversible MeSC depletion. Based on this, the article constructs an integrative model, emphasizing that future intervention strategies may need to shift from simply protecting MeSCs to preserving the temporal and spatial coupling of the HFSC–MeSC–niche network. Potential approaches may include reducing chronic niche stress, maintaining HFSC–MeSC communication, preserving ECM organization and improving the timing and strength of pro-pigmentation cues. We further propose that hair greying may provide an accessible visual readout of stem-cell niche ageing.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 10","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70365","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149106472","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":"Chronic Spontaneous Urticaria and Psychiatric Symptoms: The Blood–Brain Barrier Hypothesis","authors":"Gerasimos N. Konstantinou,&nbsp;Jerry J. Warsh,&nbsp;Daniel M. Blumberger,&nbsp;Stefan Kloiber,&nbsp;George N. Konstantinou","doi":"10.1111/exd.70369","DOIUrl":"https://doi.org/10.1111/exd.70369","url":null,"abstract":"<p>Chronic spontaneous urticaria (CSU) is a mast cell-driven inflammatory disease frequently accompanied by anxiety, depression, sleep disturbance, fatigue, and impaired quality of life. Pruritus, disturbed sleep, psychosocial burden, and treatment-related effects are established contributors to this neuropsychiatric and functional burden. Whether immune-to-brain signalling provides an additional mechanism in a susceptible subgroup remains unknown. This hypothesis-driven narrative review examines the blood–brain barrier (BBB) as one potential interface linking CSU-associated inflammation to central effects. CSU studies report systemic inflammatory, vascular, and neuroimmune signals, including cytokine signatures, circulating matrix metalloproteinase-9, and substance P–MRGPRX2-related findings. Their potential neurovascular relevance is inferred from experimental or other disease settings rather than demonstrated in CSU per se. Our targeted search identified no human CSU studies assessing regional BBB permeability with dynamic contrast-enhanced magnetic resonance imaging or tracer methods, blood–cerebrospinal fluid barrier function with the albumin quotient, serum S100B, or brain endothelial tight-junction integrity, including claudin-5 or occludin. Structural and functional neuroimaging findings in CSU do not establish barrier dysfunction. Systemic mastocytosis provides comparative evidence for mast-cell-related neuropsychiatric manifestations, although barrier involvement remains unproven. We therefore propose neurovascular alteration as a testable, non-exclusive risk modifier whose relevance to CSU pathophysiology and psychiatric symptoms remains to be established.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 10","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70369","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149068329","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":"Keratinocyte Autophagy in Inflammatory Dermatoses: Mechanisms, Disease-Specific Programs and Therapeutic Opportunities","authors":"Yulu Wang,&nbsp;Kevin M. Truong-Balderas,&nbsp;Yi Gao,&nbsp;Claudia Lasalle,&nbsp;Sabrina Schundler,&nbsp;Bethany E. Perez White,&nbsp;Kyle T. Amber,&nbsp;Adrian P. Mansini","doi":"10.1111/exd.70370","DOIUrl":"https://doi.org/10.1111/exd.70370","url":null,"abstract":"<p>Autophagy is increasingly recognised as a regulator of epithelial stress adaptation in the skin, but its role in inflammatory dermatoses remains difficult to interpret because autophagy intersects with barrier biology, keratinocyte differentiation, immune signalling, intracellular trafficking and lysosomal degradation. Keratinocytes are immune-competent epithelial cells that integrate cytokine exposure, oxidative stress, microbial sensing and tissue injury into inflammatory output. In this review, we synthesize evidence on keratinocyte autophagy as a disease-dependent regulator of epidermal homeostasis and cutaneous inflammation. We summarize core autophagy machinery, selective autophagy programs relevant to epidermal differentiation and the interpretive value of autophagic flux and lysosomal competence. We then discuss how autophagy influences keratinocyte differentiation, organelle clearance, lipid handling, barrier support, inflammatory restraint and stress adaptation. Disease-specific evidence is reviewed in psoriasis, AP1S3-associated pustular autoinflammation, atopic dermatitis and vitiligo. Across these settings, keratinocyte autophagy cannot be classified as uniformly protective or pathogenic; its effects depend on inflammatory context, trafficking state, cell-type-specific outputs and the ability of lysosomes to complete degradation. We also consider lessons from other barrier epithelia, therapeutic implications and common methodological limitations. A keratinocyte-centered, flux-aware interpretation provides a framework for organizing disease-specific autophagy biology and for designing more rigorous mechanistic studies in inflammatory dermatoses.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 10","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70370","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149068330","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":"When Cold Gets Under the Skin: An Immunometabolic Circuit in Psoriasis","authors":"Young In Lee,&nbsp;Tae-Gyun Kim","doi":"10.1111/exd.70368","DOIUrl":"https://doi.org/10.1111/exd.70368","url":null,"abstract":"<div>\u0000 \u0000 <p>Psoriasis is a common immune-mediated inflammatory disease that often worsens during cold weather, yet the mechanisms linking cold exposure to enhanced psoriatic inflammation remain poorly understood. Shuai and colleagues identify a distinct macrophage population induced by cold stress in the dermal adipose layer, characterized by heightened lipid metabolism and IL-1β production. These macrophages promote IL-17A-producing γδT-cell responses in a mouse model of psoriasis, uncovering a potential cellular mechanism through which cold environments exacerbate psoriatic inflammation via immune-metabolic pathways.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 10","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149068570","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}