Journal of dermatological science最新文献

英文中文

C-C motif chemokine receptor 7 (CCR7) in the spinal cord inhibits chronic itch through the neuropeptide NPY 脊髓C-C基序趋化因子受体7 （CCR7）通过神经肽NPY抑制慢性瘙痒。

IF 4.6

Journal of dermatological science

Pub Date : 2025-08-01 Epub Date: 2025-05-09 DOI: 10.1016/j.jdermsci.2025.05.001

Yanying Tan , Zhongqiu Zhao , Xue Luo , Xuebin Han , Hui Xiong , Zhinan Mei

Background

Studies showed that C-C motif chemokine receptor 7 (CCR7) contributes to the maintenance of neuropathic pain. However, whether CCR7 is involved in chronic itch remains unclear.

Objective

To explore the relationship between CCR7 and chronic itch.

Methods

The scratching behavior of wild-type (WT) and Ccr7^-/- mice in acute and chronic itch models, or of WT mice in chronic itch after intrathecal injection of CCR7 neutralizing antibody was compared. Mechanical, thermal, and inflammatory pain responses of Ccr7^-/- mice and WT mice were examined. The expression of CCR7, some known lamina-specific markers, and itch-related mediators in the spinal cord of WT and Ccr7^-/- mice with chronic itch were detected by immunostaining and qRT-PCR respectively. Finally, to explore the possible relationship between CCR7 and Neuropeptide Y (NPY), intrathecal injection of CCR7-siRNA for in vivo knockdown and neurotoxin bombesin-saporin for GRPR-expressing cells ablation were used.

Results

Ccr7^-/- mice displayed increasing scratching in chronic itch models. CCR7 neutralizing antibody elevated, while CCR7 ligands CCL19/CCL21 alleviated the scratching behavior in chronic itch models. However, the responses of Ccr7^-/- mice to mechanical, thermal, and inflammatory pain did not differ from their WT controls. Also, CCR7⁺ interneurons co-express NPY, and CCR7 expression was enhanced in the spinal cord of mice with chronic itch. Furthermore, spinal NPY expression was down-regulated in Ccr7^-/- mice or after CCR7-siRNA. Finally, GRPR⁺ neuron ablation eliminated scratching behavior in chronic itch mice regardless of whether the mice lacked CCR7.

Conclusion

Spinal CCR7 mediates persistent itch through a neural network with the inhibitory neuropeptide NPY.

背景：研究表明C-C基序趋化因子受体7 （CCR7）参与神经性疼痛的维持。然而，CCR7是否参与慢性瘙痒尚不清楚。目的：探讨CCR7与慢性瘙痒的关系。方法：比较野生型（WT）和Ccr7-/-小鼠急性和慢性瘙痒模型以及慢性瘙痒小鼠鞘内注射Ccr7中和抗体后的抓痕行为。研究了Ccr7-/-小鼠和WT小鼠的机械、热和炎症性疼痛反应。采用免疫染色法和qRT-PCR分别检测慢性瘙痒小鼠和慢性瘙痒小鼠脊髓中CCR7、部分已知板特异性标记物和瘙痒相关介质的表达。最后，为了探索CCR7与神经肽Y （NPY）之间的可能关系，我们使用鞘内注射CCR7- sirna进行体内敲除，并使用神经毒素炸弹素皂苷进行grpr表达细胞消融。结果：Ccr7-/-小鼠在慢性瘙痒模型中表现出增加的抓痕。CCR7中和抗体升高，CCR7配体CCL19/CCL21减轻慢性瘙痒模型的抓痕行为。然而，Ccr7-/-小鼠对机械性、热性和炎症性疼痛的反应与WT对照组没有差异。CCR7+中间神经元共表达NPY， CCR7在慢性瘙痒小鼠脊髓中的表达增强。此外，Ccr7-/-小鼠或Ccr7- sirna后脊髓NPY表达下调。最后，无论小鼠是否缺乏CCR7， GRPR+神经元消融均可消除慢性瘙痒小鼠的抓痕行为。结论：脊髓CCR7通过抑制神经肽NPY的神经网络介导持续瘙痒。

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引用次数: 0

The joint meeting of the annual symposiums for KSSBR and PAPSBRS: Let's learn from its success for further development of skin barrier research KSSBR与PAPSBRS年度研讨会联席会议：让我们借鉴其成功经验，进一步发展皮肤屏障研究。

IF 4.6

Journal of dermatological science

Pub Date : 2025-07-01 Epub Date: 2025-04-28 DOI: 10.1016/j.jdermsci.2025.04.008

Yutaka Hatano , Yoshikazu Uchida , Takuya Takeichi

引用次数: 0

Editors Choice 编辑的选择

IF 4.6

Journal of dermatological science

Pub Date : 2025-07-01 Epub Date: 2025-06-24 DOI: 10.1016/S0923-1811(25)00106-9

引用次数: 0

Big data-driven target identification by machine learning: DRD2 as a therapeutic target for psoriasis 机器学习大数据驱动的靶标识别：DRD2作为银屑病的治疗靶标。

IF 4.6

Journal of dermatological science

Pub Date : 2025-07-01 Epub Date: 2025-04-26 DOI: 10.1016/j.jdermsci.2025.04.012

Takashi Sakai , Ryusuke Sawada , Otoha Ichinose , Takeshi Terabayashi , Yutaka Hatano , Yoshihiro Yamanishi , Toshimasa Ishizaki

Background

The development of medical treatments has traditionally relied on researchers leveraging scientific knowledge to hypothesize disease mechanisms and identify therapeutic agents. However, the depletion of novel therapeutic targets has become a significant challenge, resulting in stagnation within pharmaceutical research.

Objective

To address the scarcity of therapeutic targets, we developed a machine learning (ML)-based system capable of predicting therapeutic target molecules for diseases. To validate its utility, we applied this system to psoriasis, aiming to identify novel treatment strategies.

Methods

Our approach utilized a large clinical database to calculate reporting odds ratios for all drugs associated with the prevention of diseases of interest. We identified target proteins by analyzing large chemical structure databases to discover proteins commonly associated with preventive drug candidates. Experimental validation was conducted by administering a predicted therapeutic candidate in an imiquimod-induced psoriasis mouse model.

Results

The ML-based predictions identified drugs for Parkinson’s disease as potential preventive candidates for psoriasis. Further analysis highlighted dopamine receptor D2 (DRD2) as a therapeutic target. Administration of a DRD2 agonist alleviated psoriasis symptoms in mice, evidenced by the downregulation of mRNA expression in the IL-17 pathway and reduced serum tumor necrosis factor-α levels.

Conclusion

This study demonstrates the utility of a novel ML-based system for identifying therapeutic targets, as shown by its successful application in uncovering the role of DRD2 in psoriasis. Beyond psoriasis, this system offers significant potential for exploring pathological mechanisms and discovering therapeutic targets across various diseases.

背景：医学治疗的发展传统上依赖于研究人员利用科学知识来假设疾病机制和确定治疗剂。然而，新的治疗靶点的枯竭已经成为一个重大挑战，导致药物研究停滞不前。目的：为了解决治疗靶标缺乏的问题，我们开发了一个基于机器学习（ML）的系统，能够预测疾病的治疗靶标分子。为了验证其实用性，我们将该系统应用于牛皮癣，旨在确定新的治疗策略。方法：我们的方法利用一个大型临床数据库来计算所有与相关疾病预防相关的药物的报告优势比。我们通过分析大型化学结构数据库来确定靶蛋白，以发现与预防性候选药物通常相关的蛋白质。通过在吡喹莫德诱导的牛皮癣小鼠模型中施用预测的治疗候选物进行实验验证。结果：基于ml的预测确定了帕金森病的药物作为牛皮癣的潜在预防候选药物。进一步的分析强调了多巴胺受体D2 （DRD2）作为治疗靶点。通过下调IL-17通路mRNA表达和降低血清肿瘤坏死因子-α水平，DRD2激动剂可缓解小鼠银屑病症状。结论：本研究证明了一种新的基于ml的系统在识别治疗靶点方面的实用性，该系统成功地揭示了DRD2在牛皮癣中的作用。除银屑病外，该系统还具有探索各种疾病的病理机制和发现治疗靶点的巨大潜力。

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引用次数: 0

Algae ferment regulates initiation, amplification, and resolution of inflammation 藻类发酵调节炎症的发生、扩大和消退。

IF 4.6

Journal of dermatological science

Pub Date : 2025-07-01 Epub Date: 2025-04-09 DOI: 10.1016/j.jdermsci.2025.04.005

Jaime Emmetsberger , Donald Collins , Nevena Karaman-Jurukovska , Amanda Messina , Dawn Layman , Thomas Mammone , Kenji Kabashima , Nadine Pernodet

引用次数: 0

Scratching, not dryness, drives key skin changes in the AEW-induced dry skin pruritus model, highlighting the importance of breaking itch-scratch cycle in chronic pruritus 在aew诱导的干性皮肤瘙痒模型中，驱动关键皮肤变化的是抓挠，而不是干燥，这突出了在慢性瘙痒中打破痒-抓循环的重要性。

IF 4.6

Journal of dermatological science

Pub Date : 2025-07-01 Epub Date: 2025-04-09 DOI: 10.1016/j.jdermsci.2025.04.004

Atsuko Funakoshi , Tetsuya Honda

引用次数: 0

PRRX1 is a key regulator in the phenotypic transition between human normal dermal and keloid fibroblasts PRRX1是人类正常真皮和瘢痕疙瘩成纤维细胞表型转换的关键调节因子。

IF 4.6

Journal of dermatological science

Pub Date : 2025-07-01 Epub Date: 2025-05-16 DOI: 10.1016/j.jdermsci.2025.05.002

Shuqian Dou , Fengyu Zhang , Yongjing He , Pan Du , Yue Deng , Mingkun Shao , Guoxun Yang , Kongjia Wu , Yueqin Zeng , Cheng Peng , Wenjun Liu

Background

Scarring after skin trauma is a major clinical challenge, as it affects patients’ appearance and function.

Objective

Given that human foetal skin possesses scarless wound healing ability, we aimed to understand the differences among human foetal skin, postnatal skin, and keloid tissue to find out the key factors affecting wound healing outcome.

Methods

We used spatial transcriptomics (ST), histological imaging, and other methods to investigate the cellular and molecular characteristics underlying scarless healing by comparing these skin types.

Results

We identified histological and cellular differences among these samples, including the extracellular matrix, hair follicles, stem cells, and immune cells. Significant heterogeneity was found in fibroblasts across all samples. Among these fibroblast subpopulations, the proportion of paired related homeobox 1 (PRRX1)-positive fibroblast increased from foetus to postnatal skin (PS) and further in keloids. We validated PRRX1’s roles in regulating the phenotypic transition between normal and keloid fibroblasts. A three-dimensional human keloid model was used to further confirm its roles at the tissue level.

Conclusions

In summary, our work explores the unique characteristics of foetal skin and identifies an important transcription factor in regulating scarless healing, which provides the translational potential for future clinical treatments aimed at promoting scarless wound healing.

背景：皮肤创伤后瘢痕形成是一个重大的临床挑战，因为它影响患者的外观和功能。目的：鉴于人类胎儿皮肤具有无疤痕的创面愈合能力，我们旨在了解人类胎儿皮肤与出生后皮肤和瘢痕疙瘩组织的差异，找出影响创面愈合结果的关键因素。方法：通过比较这些皮肤类型，我们使用空间转录组学（ST）、组织学成像和其他方法来研究无疤痕愈合背后的细胞和分子特征。结果：我们确定了这些样本之间的组织学和细胞差异，包括细胞外基质、毛囊、干细胞和免疫细胞。在所有样本的成纤维细胞中发现了显著的异质性。在这些成纤维细胞亚群中，配对相关同源盒1 （PRRX1）阳性成纤维细胞的比例从胎儿到出生后皮肤（PS）增加，在瘢痕疙瘩中进一步增加。我们验证了PRRX1在调节正常瘢痕疙瘩成纤维细胞和瘢痕疙瘩成纤维细胞之间的表型转变中的作用。使用三维人体瘢痕疙瘩模型进一步确认其在组织水平上的作用。结论：总之，我们的工作探索了胎儿皮肤的独特特征，并确定了调节无疤痕愈合的重要转录因子，这为未来旨在促进无疤痕伤口愈合的临床治疗提供了转化潜力。

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引用次数: 0

BAFF modulates T follicular helper cell differentiation through the BAFFR-PI3K/AKT-mTOR signaling pathway in bullous pemphigoid BAFF通过BAFFR-PI3K/AKT-mTOR信号通路调节T滤泡辅助细胞在大疱性类天疱疮中的分化。

IF 4.6

Journal of dermatological science

Pub Date : 2025-07-01 Epub Date: 2025-04-15 DOI: 10.1016/j.jdermsci.2025.04.006

Liang Li , Hui Fang , Shengxian Shen , Kang Li, Zhiguo Li, Haijun Miao, Xia Li, Shuai Shao, Erle Dang, Gang Wang, Hongjiang Qiao

Background

Bullous pemphigoid (BP) is an autoimmune blistering disease primarily affecting older individuals. B-cell activating factor (BAFF), a member of the tumor necrosis factor superfamily, is crucial for B cell survival and T cell function. However, its role in the development of BP remains unclear.

Objective

To explore the BAFF expression and its specific role in the pathogenesis of BP.

Methods

BAFF levels in the serum, skin lesions, and blister fluid (BF) were measured using enzyme-linked immunosorbent assay, immunofluorescence, and flow cytometry. Naïve CD4⁺ T cells derived from healthy volunteers were cultured with BAFF to evaluate T cell activation, proliferation, and differentiation in vitro. A BP-like mouse model was constructed using BP180 immunization to analyze the therapeutic effects of anti-BAFF monoclonal antibody (mAb).

Results

BAFF levels were elevated in the serum, BF, and skin lesions of patients with BP, and the BAFF levels in the serum and BF were correlated with disease severity. Additionally, monocytes, neutrophils, and eosinophils were the likely sources of BAFF in the circulation and skin lesions of BP patients. In vitro, BAFF facilitated the activation and differentiation of naïve CD4⁺ T cells into T follicular helper cells (Tfh). Moreover, BAFF mediated Tfh differentiation via the BAFF receptor (BAFFR)-PI3K/AKT-mTOR pathway. Anti-BAFF mAb treatment reduced both the proportions of Tfh cells and autoantibody production in vivo.

Conclusion

These findings suggested that BAFF mediated Tfh differentiation via the BAFFR-PI3K/AKT-mTOR pathway, highlighting its promise as a therapeutic target for the management of BP.

背景：大疱性类天疱疮（BP）是一种主要影响老年人的自身免疫性水疱疾病。B细胞活化因子（BAFF）是肿瘤坏死因子超家族的一员，对B细胞存活和T细胞功能至关重要。然而，它在英国石油公司的发展中所扮演的角色仍不清楚。目的：探讨BAFF的表达及其在BP发病中的特殊作用。方法：采用酶联免疫吸附法、免疫荧光法和流式细胞术检测血清、皮损和水疱液（BF）中的BAFF水平。Naïve来源于健康志愿者的CD4+ T细胞与BAFF一起培养，以评估T细胞的体外活化、增殖和分化。采用BP180免疫构建bp样小鼠模型，分析抗baff单克隆抗体（mAb）的治疗效果。结果：BP患者血清、BF和皮损中BAFF水平升高，且血清和BF中BAFF水平与疾病严重程度相关。此外，单核细胞、中性粒细胞和嗜酸性粒细胞可能是BP患者循环和皮肤病变中BAFF的来源。在体外，BAFF促进naïve CD4+ T细胞向T滤泡辅助细胞（Tfh）的活化和分化。此外，BAFF通过BAFF受体(BAFFR)-PI3K/AKT-mTOR途径介导Tfh分化。抗baff单抗处理降低了体内Tfh细胞的比例和自身抗体的产生。结论：这些发现表明BAFF通过BAFFR-PI3K/AKT-mTOR通路介导Tfh分化，突出了其作为BP治疗靶点的前景。

{"title":"BAFF modulates T follicular helper cell differentiation through the BAFFR-PI3K/AKT-mTOR signaling pathway in bullous pemphigoid","authors":"Liang Li , Hui Fang , Shengxian Shen , Kang Li, Zhiguo Li, Haijun Miao, Xia Li, Shuai Shao, Erle Dang, Gang Wang, Hongjiang Qiao","doi":"10.1016/j.jdermsci.2025.04.006","DOIUrl":"10.1016/j.jdermsci.2025.04.006","url":null,"abstract":"<div><h3>Background</h3><div>Bullous pemphigoid (BP) is an autoimmune blistering disease primarily affecting older individuals. B-cell activating factor (BAFF), a member of the tumor necrosis factor superfamily, is crucial for B cell survival and T cell function. However, its role in the development of BP remains unclear.</div></div><div><h3>Objective</h3><div>To explore the BAFF expression and its specific role in the pathogenesis of BP.</div></div><div><h3>Methods</h3><div>BAFF levels in the serum, skin lesions, and blister fluid (BF) were measured using enzyme-linked immunosorbent assay, immunofluorescence, and flow cytometry. Naïve CD4<sup>+</sup> T cells derived from healthy volunteers were cultured with BAFF to evaluate T cell activation, proliferation, and differentiation <em>in vitro</em>. A BP-like mouse model was constructed using BP180 immunization to analyze the therapeutic effects of anti-BAFF monoclonal antibody (mAb).</div></div><div><h3>Results</h3><div>BAFF levels were elevated in the serum, BF, and skin lesions of patients with BP, and the BAFF levels in the serum and BF were correlated with disease severity. Additionally, monocytes, neutrophils, and eosinophils were the likely sources of BAFF in the circulation and skin lesions of BP patients. <em>In vitro</em>, BAFF facilitated the activation and differentiation of naïve CD4<sup>+</sup> T cells into T follicular helper cells (Tfh). Moreover, BAFF mediated Tfh differentiation <em>via</em> the BAFF receptor (BAFFR)-PI3K/AKT-mTOR pathway. Anti-BAFF mAb treatment reduced both the proportions of Tfh cells and autoantibody production <em>in vivo</em>.</div></div><div><h3>Conclusion</h3><div>These findings suggested that BAFF mediated Tfh differentiation <em>via</em> the BAFFR-PI3K/AKT-mTOR pathway, highlighting its promise as a therapeutic target for the management of BP.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"119 1","pages":"Pages 18-27"},"PeriodicalIF":4.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144015560","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}

引用次数: 0

The role of PPARs family members in acne ppar家族成员在痤疮中的作用。

IF 4.6

Journal of dermatological science

Pub Date : 2025-07-01 Epub Date: 2025-05-23 DOI: 10.1016/j.jdermsci.2025.04.003

Shaoyang Zhang , Yating Yang , Li Yang, Fangyu Meng, Yizhe Mu, Yuhang Yuan, Yuan Zhang

Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that play a crucial role in the genetic regulation of lipid metabolism and energy homeostasis. There is increasing evidence to suggest that PPARs may have a significant impact on the development and progression of acne, including its role in regulating lipid production, inhibiting keratinocyte proliferation, and reducing acne-related inflammation. As such, PPARs present themselves as promising therapeutic targets for both the prevention and treatment of acne. This article provides an overview of the role of PPARs in the pathological processes underlying acne, with particular emphasis on inflammation and lipid regulation.

过氧化物酶体增殖体激活受体（PPARs）是配体激活的转录因子，在脂质代谢和能量稳态的遗传调控中起着至关重要的作用。越来越多的证据表明，ppar可能对痤疮的发生和发展有重要影响，包括其调节脂质产生、抑制角化细胞增殖和减少痤疮相关炎症的作用。因此，ppar作为预防和治疗痤疮的有希望的治疗靶点。本文概述了ppar在痤疮病理过程中的作用，特别强调炎症和脂质调节。

引用次数: 0

Editors Choice 编辑的选择

IF 4.6

Journal of dermatological science

Pub Date : 2025-06-01 Epub Date: 2025-06-06 DOI: 10.1016/S0923-1811(25)00089-1

引用次数: 0

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