Journal of dermatological science最新文献

{"title":"Regulatory role of autophagy in epidermal function","authors":"Dongyun Lei,&nbsp;Shiying Li,&nbsp;Litao Zhang,&nbsp;Guoqiang Zhang,&nbsp;Mao-Qiang Man","doi":"10.1016/j.jdermsci.2026.07.003","DOIUrl":"10.1016/j.jdermsci.2026.07.003","url":null,"abstract":"<div><div>Autophagy, a highly conserved cellular degradation process, is essential for maintaining cellular homeostasis and responding to stress. Recent studies have highlighted the importance of autophagy in regulating epidermal functions, including keratinocyte differentiation and proliferation, epidermal lipid synthesis, inflammation, and antioxidation. In the epidermis, autophagy facilitates the removal of damaged organelles and protein aggregates, ensuring proper keratinocyte maturation and stratum corneum formation. Dysregulation of autophagy has been linked to various dermatological conditions, such as psoriasis, atopic dermatitis, and skin aging. Furthermore, autophagy modulates the inflammatory response in the skin by regulating cytokine production and immune cell activity. This review summarizes evidence supporting the role of autophagy in epidermal function and emphasizes its potential as a therapeutic target. Additionally, approaches to enhance autophagy are discussed.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"124 1","pages":"Pages 1-6"},"PeriodicalIF":4.6,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148564162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial metabolic plasticity in infantile hemangioma: evidence strength, disease phase and therapeutic readiness.","authors":"Qian Lin, Ruonan Ke, Xuejun Ni, Lu Chen, Xiaofen Wan, Xiuying Shan, Biao Wang, Beichen Cai","doi":"10.1016/j.jdermsci.2026.09.003","DOIUrl":"https://doi.org/10.1016/j.jdermsci.2026.09.003","url":null,"abstract":"<p><p>Endothelial metabolism is increasingly used to explain the growth, involution and drug response of infantile hemangioma (IH), but the supporting studies differ sharply in disease relevance and validation depth. We assessed which endothelial metabolic and plasticity mechanisms are sufficiently supported to guide experiments, biomarker work or therapeutic development. We performed a structured narrative search of PubMed/MEDLINE from inception to 28 July 2026 and hand-searched the references of included studies and recent reviews. Evidence was weighted by phase-resolved human tissue, patient-derived hemangioma endothelial or stem cells, pathway-specific perturbation, orthogonal or rescue experiments, and lesion-relevant in vivo testing. PFKFB3-supported glycolysis has the most complete preclinical chain for proliferative hemangioma endothelial cells. The SOX18-mevalonate pathway is comparably well anchored during hemangioma stem-cell endothelial differentiation and supports a beta-adrenergic-receptor-independent mechanism for R(+) propranolol. AIBP/NAXE-cholesterol-HIF-1α signaling is supported by bidirectional perturbation and several animal contexts, whereas amino-acid findings remain descriptive. Endothelial-to-mesenchymal transition is not a single involution program: TGF-β1 can drive a proangiogenic state, whereas M1-associated cytokines confer mesenchymal and adipogenic competence in regression-linked models. Recent mitochondrial-targeting and cell-fate studies remain single-study, model-limited evidence. None of the proposed PFKFB3 inhibitors, statins, optically pure R(+) beta-blocker enantiomers or phase-matched combinations has established efficacy or safety for infants with IH. Current evidence prioritizes mechanisms for preclinical development, not off-label treatment. Reproducibility, infant-relevant pharmacology, developmental safety and phase-specific biomarkers are required before clinical testing.</p>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149198218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct migration behaviors of monocyte-derived versus resident langerhans cells drive the pathogenesis of imiquimod-induced skin inflammation.","authors":"Zhen Cai, Jiajia Lan, Shiyi Yan, Biling Jiang, Yuting Xia, Liang Zhao, Naming Wu, Liyun Dong, Yan Li, Jun Li, Juan Tao","doi":"10.1016/j.jdermsci.2026.08.006","DOIUrl":"https://doi.org/10.1016/j.jdermsci.2026.08.006","url":null,"abstract":"<p><strong>Background: </strong>Langerhans cells (LCs) consist of embryonically derived resident LCs (rLCs) and monocyte-derived LCs (moLCs), yet how distinct LC subsets migrate and function during psoriatic skin inflammation remains incompletely understood.</p><p><strong>Objective: </strong>To characterize the migratory behavior and immunological roles of rLCs and moLCs in imiquimod (IMQ)-induced skin inflammation.</p><p><strong>Methods: </strong>We examined LC subset dynamics in an IMQ-induced murine dermatitis model using flow cytometry and immunofluorescence. To dissect subset-specific functions, moLCs were selectively ablated in Cd207^fl/flLyz2^Cre conditional knockout mice, while rLCs were depleted using Langerin-DTR mice. Skin inflammation severity, T cell profiles, and PD-L1 expression were assessed. Human psoriatic lesions (mild vs. moderate-to-severe) were analyzed by multiplex immunofluorescence.</p><p><strong>Results: </strong>IMQ treatment induced progressive moLC accumulation in skin lesions (both number and proportion increased), while rLCs diminished locally but accumulated significantly in draining lymph nodes with upregulated CCR7 expression. Genetic ablation of moLCs reduced epidermal hyperplasia, ear thickness, and IL-17/IL-22-producing CD4⁺ T cells and γδ T cells in lesions. Conversely, rLC depletion exacerbated dermatitis, reduced PD-L1 expression in lymph node LCs, and enhanced γδ T cell activation both locally and systemically. In human psoriatic lesions, moLC density correlated with local lesion severity at the histological level, while CCR7 expression was predominantly detected on rLCs rather than moLCs.</p><p><strong>Conclusion: </strong>rLCs and moLCs display distinct migratory behaviors and exert divergent immunological functions during IMQ-induced skin inflammation. Lesion-retained moLCs are associated with local inflammatory responses, whereas lymph node-migratory rLCs are linked to immunoregulatory activity.</p>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149032106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Skin macrophage subsets in health and disease.","authors":"Felix G P Weninger, Yuki Honda Keith","doi":"10.1016/j.jdermsci.2026.09.002","DOIUrl":"https://doi.org/10.1016/j.jdermsci.2026.09.002","url":null,"abstract":"<p><p>Macrophages are heterogeneous tissue-resident immune cells distributed throughout the body. The majority of tissue-resident macrophages are seeded in the peripheral tissues during embryogenesis, and these embryonic precursors form tissue-specific macrophages dependent on their specific microenvironment. The skin is the first line of immune defence and contains various uniquely differentiated tissue-resident macrophage populations, including Langerhans cells in the epidermis, perivascular and sensory nerve-associated macrophages in the dermis, and LYVE1 + and CD169 + macrophages in the hypodermis. Cutaneous melanoma is the most aggressive skin cancer, and macrophages are abundant immune cells found in these tumours. Due to the diversity of macrophage subsets in the skin, macrophages have highly heterogeneous roles in melanoma lesions, including exerting both tumour-suppressing and promoting functions. Additionally, macrophage subsets in the tumour-draining lymph node play important roles in tumour immunity and progression. A comprehensive understanding of the different macrophage subsets in both tumour and tumour-draining lymph nodes may lead to improved therapeutic outcomes for cutaneous melanoma.</p>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149120774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatial transcriptomic profiling of selected facial cutaneous lupus erythematosus and rosacea with overlapping features.","authors":"Tae Min Kim, Yookyung Sophie Chun, Joong Heon Suh, Yun-Hui Jeon, Cheol Lee, Seon-Pil Jin, Soyun Cho","doi":"10.1016/j.jdermsci.2026.09.001","DOIUrl":"https://doi.org/10.1016/j.jdermsci.2026.09.001","url":null,"abstract":"<p><strong>Background: </strong>Cutaneous lupus erythematosus (cLE) and rosacea are generally distinct clinicopathological entities, but selected facial inflammatory presentations may show overlapping features. Molecular biomarkers may provide adjunctive information in such equivocal cases.</p><p><strong>Objective: </strong>To identify candidate molecular biomarkers distinguishing cLE from rosacea using spatial profiling techniques.</p><p><strong>Methods: </strong>FFPE skin biopsy samples from cLE and rosacea patients were analyzed using GeoMx™ Digital Spatial Profiling platform. Differentially expressed genes were identified, and pathway analysis was conducted. Candidate biomarkers were validated using immunofluorescence. An exploratory logistic regression model was developed using selected biomarkers and evaluated with leave-one-out cross-validation.</p><p><strong>Results: </strong>ISG15 and OASL were upregulated in cLE, whereas TMEM9, MOCS3, SPNS2, and TMCO1 were elevated in rosacea at both transcriptomic and protein levels. Logistic regression selected OASL, ISG15, TMEM9, and MOCS3 as a four-marker exploratory panel, which showed preliminary within-cohort discriminatory value in leave-one-out cross-validation but was not externally validated. In two diagnostically ambiguous cases, biomarker staining profiles were concordant with subsequent clinical course.</p><p><strong>Conclusion: </strong>Spatial transcriptomic profiling identified candidate biomarkers that may serve as molecular adjuncts for distinguishing rosacea from selected facial cLE cases, predominantly ACLE/SCLE in this cohort. These findings are exploratory and require validation in larger independent cohorts, including broader cLE subtypes, before clinical application.</p>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149120791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enfortumab vedotin-related cutaneous toxicity: Clinical features, pathogenesis and management.","authors":"Kazumasa Oya","doi":"10.1016/j.jdermsci.2026.08.009","DOIUrl":"https://doi.org/10.1016/j.jdermsci.2026.08.009","url":null,"abstract":"<p><p>Therapeutic strategies for malignant tumors have advanced substantially, and antibody-drug conjugates (ADCs) now enable selective delivery of cytotoxic payloads to tumor cells. Enfortumab vedotin (EV) is a nectin-4-directed ADC composed of a fully human monoclonal antibody against nectin-4 conjugated, via a protease-cleavable linker, to the microtubule-disrupting agent monomethyl auristatin E. EV has demonstrated robust antitumor activity in urothelial carcinoma and is being investigated in other nectin-4-expressing tumors. Because nectin-4 is expressed in keratinocytes and cutaneous appendages, cutaneous adverse events are among the most frequent toxicities. EV-related cutaneous toxicity represents an on-target, mechanism-based toxicity that is distinct from the cutaneous adverse events associated with conventional cytotoxic chemotherapy. This review summarizes the molecular structure and function of nectin-4 and the clinical and histopathologic features of EV-related cutaneous toxicity and discusses current approaches to management. By integrating mechanistic insights from experimental studies with clinical and histopathologic observations, this review provides a translational framework to support optimal recognition and management of EV-related cutaneous toxicity.</p>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148993351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunoglobulin deposition and plasma cell infiltration define distinct immunopathological patterns in skin diseases.","authors":"Mariko Ogawa-Momohara, Yukihiro Ozawa, Yuta Yamashita","doi":"10.1016/j.jdermsci.2026.08.011","DOIUrl":"https://doi.org/10.1016/j.jdermsci.2026.08.011","url":null,"abstract":"<p><p>Immunoglobulin deposition in the skin is an important diagnostic and etiological feature in many skin diseases. However, the relationship between deposited immunoglobulins and the local presence of antibody-producing cells, such as B cells and plasma cells, remains poorly understood. In several autoimmune diseases, including systemic lupus erythematosus and bullous pemphigoid, marked immunoglobulin deposition is observed despite limited B-cell infiltration into the skin, suggesting that the deposited antibodies primarily originate as circulating autoantibodies. In contrast, diseases such as discoid lupus erythematosus are characterized by progressive B-cell infiltration, the formation of ectopic lymphoid tissue, and increased local antibody production within the skin. In other diseases, including dermatomyositis, a mismatch is observed between circulating autoantibodies and the subclasses of deposited immunoglobulins, suggesting the possibility of local immunoglobulin production independent of systemic reactions. In several inflammatory skin diseases, such as scleroderma, hidradenitis suppurativa, and syphilis, marked plasma cell infiltration is observed from the early stages of the disease, despite weak or irregular immunoglobulin deposition. These findings suggest that plasma cells in the skin have functions other than antibody production and may contribute to disease pathogenesis through cytokine production, immune regulation, and interaction with local tissues.</p>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advanced-stage cutaneous T-cell lymphomas show distinct immune profiles in erythroderma vs. tumor lesions.","authors":"Emry R Cohenour, Abigail Fleischli, Shannon Meledathu, Malini P Naidu, Caleb A Buell, Sumanth Chennareddy, Natalia Alkon, Constanze Jonak, Zheng Ji, Agata Kurowski, Zhihong Chen, Patrick M Brunner","doi":"10.1016/j.jdermsci.2026.08.010","DOIUrl":"10.1016/j.jdermsci.2026.08.010","url":null,"abstract":"<p><strong>Background: </strong>Advanced-stage cutaneous T-cell lymphomas (CTCL) typically manifest as either skin tumor formation or erythroderma; however, exact mechanisms of lesion formation remain insufficiently characterized.</p><p><strong>Objective: </strong>To better understand mechanisms of erythroderma vs. tumor formation in advanced-stage CTCL.</p><p><strong>Methods: </strong>We compared molecular profiles of eight erythrodermic CTCL (eCTCL) with seven tumor-stage mycosis fungoides (tMF) samples by using single-cell RNA sequencing combined with T-cell receptor sequencing, and corroborated key findings using spatial transcriptomics.</p><p><strong>Results: </strong>All samples harbored a single expanded CD4+ T-cell clone expressing TOX, IL2RG, CD27, and TCF7. While advanced-stage CTCL is generally considered a type 2-skewed disease, tMF lesions demonstrated a significantly stronger Th2/Tc2 bias than eCTCL, as evidenced by enhanced expression of CCL17 and CCL13 in myeloid cells. By contrast, eCTCL lesions displayed upregulation of several type 1-associated markers such as CXCL9. Overall, we detected considerable inter-patient heterogeneity within skin biopsies, particularly in tMF. Nonetheless, tMF consistently harbored CCL19+FDCSP+ fibroblasts and IL32+CD69+ activated B cells, phenotypes previously reported in tertiary lymphoid structure formation, alongside upregulation of multiple markers associated with vascular remodeling, angiogenesis, and extracellular matrix deposition by endothelial cells. Conversely, eCTCL exhibited higher degrees of epidermal activation and markers of anti-angiogenesis such as CXCL14 within stromal cells, which may actively counteract the development of a vertical growth phase.</p><p><strong>Conclusion: </strong>Taken together, these data provide novel insights into the pathogenesis of advanced-stage CTCL skin lesions and potential therapeutic targets.</p>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149083454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PBRM1 loss in porocarcinoma arising from poroma","authors":"K. Miyamoto,&nbsp;T. Yanagi,&nbsp;H. Nishihara,&nbsp;K. Nakamura,&nbsp;R. Iwamoto,&nbsp;T. Kawamura,&nbsp;H. Ujiie","doi":"10.1016/j.jdermsci.2026.07.007","DOIUrl":"10.1016/j.jdermsci.2026.07.007","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"123 3","pages":"Pages 154-156"},"PeriodicalIF":4.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148564192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Longitudinal BRAF ctDNA monitoring in melanoma reflects disease status and predicts relapse","authors":"Daniel Rizo-Potau,&nbsp;Anton Forniés-Mariné,&nbsp;Michelle Aguilar,&nbsp;Edgard Verdura,&nbsp;Aina Montalbán-Casafont,&nbsp;Laura Serra-García,&nbsp;Sebastian Podlipnik,&nbsp;Cristina Carrera,&nbsp;Susana Puig,&nbsp;Josep Malvehy,&nbsp;Joan Anton Puig-Butillé","doi":"10.1016/j.jdermsci.2026.07.004","DOIUrl":"10.1016/j.jdermsci.2026.07.004","url":null,"abstract":"<div><h3>Background</h3><div>Early detection of melanoma relapse after curative-intent surgery remains challenging, and routine follow-up relies on imaging and imperfect serum biomarkers.</div></div><div><h3>Objective</h3><div>To assess whether longitudinal BRAF-mutant circulating tumour DNA (ctDNA) reflects disease status and whether time-updated ctDNA detection and concentration are associated with relapse hazard during post-resection surveillance.</div></div><div><h3>Methods</h3><div>We conducted a prospective real-world cohort study including 127 AJCC stage II–IV melanoma patients with tumour-confirmed BRAF V600-mutant melanoma. We analysed 318 plasma samples. BRAF-mutant ctDNA was quantified by droplet digital PCR using the Bio-Rad <em>BRAF</em> V600 Screening Kit. Disease status was classified as no evidence of disease (NED), locoregional disease, or metastatic disease. Serial ctDNA detection was analysed using logistic generalised estimating equations. In the post-resection surveillance cohort, relapse-free interval was analysed from the first post-resection surveillance sample using time-dependent Cox models with ctDNA updated serially.</div></div><div><h3>Results</h3><div>ctDNA detection was higher in locoregional disease (OR 5.90, 95% CI 2.34–14.88; P &lt; 0.001) and metastatic disease (OR 7.21, 95% CI 2.86–18.21; P &lt; 0.001) than in NED. During post-resection surveillance, detectable ctDNA (HR 17.17, 95% CI 6.12–48.14; P &lt; 0.001) and higher ctDNA concentration (HR 1.53 per doubling, 95% CI 1.36–1.71; P &lt; 0.001) were associated with increased relapse hazard.</div></div><div><h3>Conclusion</h3><div>Longitudinal BRAF p.V600E/K/R ctDNA monitoring reflects disease status and identifies surveillance intervals with increased relapse risk, despite limited sensitivity. These findings support further refinement of ctDNA-based approaches to complement standard melanoma follow-up.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"123 3","pages":"Pages 133-140"},"PeriodicalIF":4.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148632782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}