JOURNAL OF DERMATOLOGICAL SCIENCE皮肤病学科学杂志
JOURNAL OF DERMATOLOGICAL SCIENCE(英文缩写 J DERMATOL SCI),ISSN 0923-1811,eISSN 1873-569X,中文译名:皮肤病学科学杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 5.408 | Q1 |
| 2022 | 4.600 | Q1 |
| 2023 | 3.800 | Q1 |
| 2024 | 4.000 | Q1 |
| 2025 | 4.600 | Q1 |
JOURNAL OF DERMATOLOGICAL SCIENCE 最新收录文献
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1. Distinct migration behaviors of monocyte-derived versus resident langerhans cells drive the pathogenesis of imiquimod-induced skin inflammation.
PMID:日期:2026-09-23Langerhans 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. To characterize the migratory behavior and immunological roles of rLCs and moLCs in imiquimod (IMQ)-induced skin inflammation. 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 Cd207Lyz2 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. 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. 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.
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2. Enfortumab vedotin-related cutaneous toxicity: Clinical features, pathogenesis and management.
PMID:日期:2026-09-03Therapeutic 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.
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3. Proteomic and metabolomic profiling reveals dysregulation of immune states, mucin-type glycosylation and steroid metabolism in extramammary Paget's disease.
PMID:日期:2026-09-01Extramammary Paget's disease is a rare cutaneous adenocarcinoma characterized by mucin-rich Paget cells and chronic inflammation, yet its molecular basis remains unclear. To systematically characterize the proteomic and metabolomic landscape of EMPD, uncover immune heterogeneity, and identify molecular pathways underlying tumor progression and microenvironment remodeling. We performed integrated proteomic and metabolomic analyses on 92 male tumor patients and 30 healthy controls, identifying 10,217 proteins and 1466 metabolites. Extramammary Paget's disease lesions exhibited broad activation of inflammatory pathways. Immune profiling further uncovered substantial inflammatory heterogeneity, delineating immune-cold and immune-hot subtypes, with the latter associated with stronger invasive potential. Aberrant mucin-type glycosylation was also prominent, featuring Tn-modified MUC1 and MUC5AC accompanied by elevated GALNT7, GALNT6, GALNT4, and ST6GAL1, which correlated with inflammatory intensity. Metabolomic data demonstrated elevated levels of testosterone, dehydroepiandrosterone, and related intermediates in tumor tissues, indicating an androgen-enriched metabolic profile in extramammary Paget's disease. These findings reveal immune, glycoproteomic, and metabolomic pathways in extramammary Paget's disease pathogenesis and provide novel insights for molecular classification and therapeutic targeting.
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4. Longitudinal BRAF ctDNA monitoring in melanoma reflects disease status and predicts relapse.
PMID:日期:2026-09-01Early detection of melanoma relapse after curative-intent surgery remains challenging, and routine follow-up relies on imaging and imperfect serum biomarkers. 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. 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 BRAF 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. ctDNA detection was higher in locoregional disease (OR 5.90, 95% CI 2.34-14.88; P < 0.001) and metastatic disease (OR 7.21, 95% CI 2.86-18.21; P < 0.001) than in NED. During post-resection surveillance, detectable ctDNA (HR 17.17, 95% CI 6.12-48.14; P < 0.001) and higher ctDNA concentration (HR 1.53 per doubling, 95% CI 1.36-1.71; P < 0.001) were associated with increased relapse hazard. 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.
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6. Inflammaging in melanoma: Precision control for optimizing immune checkpoint inhibition.
PMID:日期:2026-09-01Aging is a major risk factor for melanoma and is accompanied by a chronic, low-grade inflammatory state termed "inflammaging". Although inflammation is essential for host defense and antitumor immunity, not all inflammatory states are beneficial. Instead, inflammaging can drive immune dysfunction and impair responses to immune checkpoint inhibitors (ICIs). ICIs have revolutionized the treatment of advanced melanoma; however, durable clinical benefit is limited to a subset of patients, and immune-related adverse events remain a major challenge. These limitations highlight the need to better understand how inflammaging intersects with anti-tumor immunity and immunotherapy outcomes. In this review, we focus on key inflammaging-associated cytokines-interleukin-6 (IL-6), interleukin-1 (IL-1), and tumor necrosis factor-α (TNF-α)-and discuss their roles in shaping melanoma progression and responses to ICIs. IL-6 has emerged as a key mediator linking tumor-promoting inflammation to immune suppression and immunotherapy-related toxicity, with growing preclinical and clinical evidence supporting its selective blockade as a strategy to enhance ICI tolerability and efficacy. IL-1 signaling contributes to tumor-promoting inflammation and immune dysregulation in melanoma, although clinical evidence supporting IL-1-targeted strategies remains limited. TNF-α exhibits context-dependent effects, acting as both a mediator of anti-tumor immunity and resistance to ICIs when chronically sustained. Together, these findings support a model in which selective modulation of pathological inflammaging, rather than broad suppression of inflammation, may improve the therapeutic index of ICIs. Targeting specific cytokine pathways offers a translationally relevant strategy to optimize immunotherapy outcomes in melanoma, particularly in inflammaging-associated contexts.
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8. Imaging-guided tape stripping reveals consistent stratum corneum profiling of disease severity and treatment-responsive molecular features in pediatric atopic dermatitis.
PMID:日期:2026-09-01Atopic dermatitis (AD) is a common pediatric skin disorder with early onset and complex pathophysiology. Tape-strip sampling has enabled minimally invasive molecular profiling of skin lesions in children, yet approaches that verify and standardize stratum corneum (SC) sampling depth have remained limited. To evaluate the utility of imaging-guided tape stripping of SC, combined with transcriptomic and cytokine profiling, for characterizing molecular changes associated with disease severity and treatment response in pediatric AD. By coupling real-time imaging-guided tape stripping with RNA sequencing and cytokine profiling, we examined SC molecular signatures in healthy children (n = 15) and lesional and non-lesional skin of pediatric AD patients (n = 39) with heterogeneous disease severity, both at baseline and following 2 weeks of topical corticosteroid treatment. Using imaging-verified SC sampling, we identified robust molecular signatures, including > 1100 differentially expressed genes (DEGs) between healthy and AD skin, and 144 DEGs between lesional and non-lesional AD skin (fold-change ≥2, FDR <0.1). Lesional skin showed enrichment of type 17- and type 2-associated immune pathways, tissue remodeling, and cell cycle control. Thirteen transcripts were significantly associated with clinical severity or itch, including CXCL8/IL8, CD300A, and FPR1. Most of these transcripts decreased after corticosteroid treatment, whereas CD300A and FCGR2B/CD32 remained elevated in a subset of children. These findings support the use of real-time imaging-guided tape stripping as a standardized, minimally invasive approach for verifying SC sampling depth and monitoring molecular changes associated with disease activity and treatment response in pediatric AD.
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9. A shift towards a type I immune response in chronic atopic dermatitis favours an IL-15 dependent tissue resident memory cell niche.
9. 慢性特应性皮炎向I型免疫反应的转变有利于IL-15依赖的组织驻留记忆细胞生态位PMID:日期:2026-09-01Tissue resident memory (TRM) cells are of interest in chronic inflammatory skin diseases as they are believed to facilitate flares in the same anatomical area. IL-15 is an essential growth factor for the survival of TRM in the skin compartment. A main source of IL-15 are tissue-resident cells. The purpose of this study was to explore the role of IL-15 in the chronification process of atopic dermatitis (AD). Primary human keratinocytes and fibroblasts were cultured and exposed to a range of stimuli in order to assess their IL-15 expression and production, which were measured by qPCR and ELISA, respectively. RNAseq and PCR were performed from lesional and non-lesional atopic dermatitis (AD) biopsies. We tested a range of type I and type II response-associated cytokines and PAMPs on primary human fibroblasts and keratinocytes. The main inducer for IL-15 in keratinocytes proved to be IFNγ, while fibroblasts showed responsiveness to long-term exposure to IL-4. Transcriptomic analyses of AD skin biopsies confirmed that IL-15 was associated with a higher IFN signature and longer disease duration, and a significant correlation was observed between IL-15 and the TRM molecules CCR8 and CD69. The epidermal compartment responds to IFNs with IL-15 expression. Analysis of patient-derived skin biopsies highlights higher expression of IL-15 in the context of a Th1 shift known to occur in chronic AD. These data suggest that flares require prompt intervention to avoid consolidation of an IFNγ-driven tissue memory.
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10. Postzygotic biallelic inactivation of FDFT1 underlies solitary lesion formation in porokeratosis of Mibelli.
PMID:日期:2026-08-25Porokeratosis reflects clonal expansion of keratinocytes with biallelic inactivation of mevalonate-cholesterol biosynthesis pathway genes. In disseminated porokeratosis (DP), lesions arise through independent somatic second hits in carriers of heterozygous germline pathogenic variants, whereas porokeratosis of Mibelli (PM) is usually solitary, and its molecular basis remains incompletely defined. To elucidate the molecular basis of solitary PM. We analyzed blood and lesional epidermis from seven patients with solitary PM within a 156-patient porokeratosis cohort using deep sequencing, copy-number/SNP profiling, and methylation analysis. Solitary PM plaques were larger and more irregular than the annular DP lesions. No pathogenic germline variants were detected in MVK, PMVK, MVD, FDPS, or FDFT1. Three patients had somatic biallelic genetic inactivation of FDFT1 through putative deleterious variants and/or focal microdeletions. The remaining four showed FDFT1 promoter hypermethylation with loss of heterozygosity (LOH) at the FDFT1 locus due to copy-neutral LOH or a monoallelic 8p deletion, consistent with early monoallelic epigenetic silencing, followed by genetic loss of the remaining active allele. In one patient, part of the plaque expanded centrifugally over 7.5 years. Solitary PM can be driven by postzygotic, lesion-restricted, biallelic inactivation of FDFT1 through genetic or epigenetic mechanisms within a single epidermal clone, promoting clonal expansion. This model may explain the tendency toward solitary PM lesions. The low probability of acquiring postzygotic biallelic inactivation without germline predisposition may underlie solitary PM and suggest a low recurrence risk for offspring, unlike DP driven by germline heterozygosity.