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Montagna Symposium on the Biology of Skin 70th Anniversary: Visualizing the Future! 蒙塔格纳皮肤生物学研讨会 70 周年:展望未来!
IF 5.7 2区 医学 Q1 DERMATOLOGY Pub Date : 2024-08-21 DOI: 10.1016/j.jid.2024.04.001
Dennis R. Roop , Thomas Krieg , Sabine Werner , Stuart Yuspa , Kyra Diehl , Riyad Seervai , Tamia Harris-Tryon , Sancy A. Leachman
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引用次数: 0
The 2023 PXE Calcification Meeting in Budapest: A Focus on Clinical Trials for this Disease 2023 年布达佩斯 PXE 钙化会议:关注该疾病的临床试验。
IF 5.7 2区 医学 Q1 DERMATOLOGY Pub Date : 2024-08-17 DOI: 10.1016/j.jid.2024.06.1283
Viola Pomozi , Sharon F. Terry , András Váradi
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引用次数: 0
The Central Roles of Keratinocytes in Coordinating Skin Immunity 角质形成细胞在协调皮肤免疫中的核心作用
IF 5.7 2区 医学 Q1 DERMATOLOGY Pub Date : 2024-08-08 DOI: 10.1016/j.jid.2024.06.1280
Jared Simmons , Richard L. Gallo
The function of keratinocytes (KCs) to form a barrier and produce cytokines is well-known, but recent progress has revealed many different roles for KCs in regulation of skin immunity. In this review, we provide an update on the current understanding of how KCs communicate with microbes, immunocytes, neurons, and other cells to form an effective immune barrier. We catalog the large list of genes and metabolites of KCs that participate in host defense and discuss the mechanisms of immune crosstalk, addressing how KCs simultaneously form a physical barrier, communicate with fibroblasts, and control immune signals. Overall, the signals sent and received by KCs are an exciting group of therapeutic targets to explore in the treatment of dermatologic disorders.
众所周知,角质形成细胞(KCs)具有形成屏障和产生细胞因子的功能,但最近的研究进展揭示了 KCs 在调节皮肤免疫方面的多种不同作用。在这篇综述中,我们将介绍目前对 KC 如何与微生物、免疫细胞、神经元和其他细胞沟通以形成有效免疫屏障的最新认识。我们列出了参与宿主防御的大量 KC 基因和代谢产物,并讨论了免疫串扰的机制,探讨了 KC 如何同时形成物理屏障、与成纤维细胞沟通并控制免疫信号。总之,KCs 发出和接收的信号是治疗皮肤病的一组令人兴奋的治疗目标。
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引用次数: 0
Mechanistic Basis for the Translation Inhibition of Cutibacterium acnes by Clindamycin 克林霉素抑制痤疮棒状杆菌翻译的机制基础
IF 5.7 2区 医学 Q1 DERMATOLOGY Pub Date : 2024-08-08 DOI: 10.1016/j.jid.2024.07.013
Ivan B. Lomakin , Swapnil C. Devarkar , Ayman Grada , Christopher G. Bunick
Inflammation and the Gram-positive anaerobic bacterium Cutibacterium acnes, which is implicated in acne pathogenesis and pilosebaceous-unit inflammation, are the main targets of antibiotic-based therapy against acne vulgaris (acne). The most widely used antibiotics in acne therapy are tetracyclines, macrolides, and lincosamides. Unfortunately, C. acnes bacteria over the past several decades have demonstrated increased resistance to these antibiotics, particularly to clindamycin. The precise knowledge of how antibiotics interact with their clinical target is needed to overcome this problem. Toward this goal, we determined the structure of clindamycin in complex with the ribosome of C. acnes at 2.53 Å resolution using cryogenic electron microscopy. The galactose sugar moiety of clindamycin interacts with nucleotides of the 23S ribosomal RNA directly or through a conserved network of water-mediated interactions. Its propyl pyrrolidinyl group interacts with the 23S ribosomal RNA through van der Waals forces. Clindamycin binding to the C. acnes ribosome interferes with both: proper orientation of the aminoacyl group of the A-site bound transfer RNA that is needed for peptide bond formation and with the extension of the nascent peptide. Our data are important for advancing the understanding of antibiotic resistance and development of narrow-spectrum antibacterial drugs, which is an urgent need for contemporary antibiotic stewardship.
炎症和革兰氏阳性厌氧菌痤疮丙酸杆菌(Cutibacterium acnes)是抗生素治疗寻常性痤疮(痤疮)的主要目标。痤疮治疗中最广泛使用的抗生素是四环素类、大环内酯类和林可酰胺类。遗憾的是,在过去几十年中,痤疮丙酸杆菌对这些抗生素的耐药性不断增强,尤其是对克林霉素。要解决这一问题,就必须准确了解抗生素与其临床目标之间的相互作用。为此,我们利用低温电子显微镜以 2.53 Å 的分辨率测定了克林霉素与痤疮棒状杆菌核糖体的复合物结构。克林霉素的半乳糖糖基与 23S rRNA 的核苷酸直接或通过水介导的保守网络相互作用。其丙基吡咯烷基团通过范德华力与 23S rRNA 相互作用。克林霉素与痤疮棒状杆菌核糖体的结合既会干扰肽键形成所需的 A 位点结合 tRNA 氨基酰基的正确方向,也会干扰新生肽的延伸。我们的数据对于促进对抗生素耐药性的了解和窄谱抗菌药物的开发非常重要,这是当代抗生素管理的迫切需要。
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引用次数: 0
Bone Marrow–Derived ABCC6 Is an Essential Regulator of Ectopic Calcification In Pseudoxanthoma Elasticum 骨髓衍生的 ABCC6 是 PXE 异位钙化的重要调节因子
IF 5.7 2区 医学 Q1 DERMATOLOGY Pub Date : 2024-08-01 DOI: 10.1016/j.jid.2024.01.026

Physiological calcification of soft tissues is a common occurrence in aging and various acquired and inherited disorders. ABCC6 sequence variations cause the calcification phenotype of pseudoxanthoma elasticum (PXE) as well as some cases of generalized arterial calcification of infancy, which is otherwise caused by defective ENPP1. ABCC6 is primarily expressed in the liver, which has given the impression that the liver is central to the pathophysiology of PXE/generalized arterial calcification of infancy. The emergence of inflammation as a contributor to the calcification in PXE suggested that peripheral tissues play a larger role than expected. In this study, we investigated whether bone marrow–derived ABCC6 contributes to the calcification in PXE. In Abcc6‒/‒ mice, we observed prevalent mineralization in several lymph nodes and surrounding connective tissues and an extensive network of lymphatic vessels within vibrissae, a calcified tissue in Abcc6‒/‒ mice. Furthermore, we found evidence of lymphangiogenesis in patients with PXE and mouse skin, suggesting an inflammatory process. Finally, restoring wild-type bone marrow in Abcc6‒/‒ mice produced a significant reduction of calcification, suggesting that the liver alone is not sufficient to fully inhibit mineralization. With evidence that ABCC6 is expressed in lymphocytes, we suggest that the adaptative immune system and inflammation largely contribute to the calcification in PXE/generalized arterial calcification of infancy.

软组织的生理性钙化是衰老以及各种获得性和遗传性疾病的常见现象。ABCC6序列变异会导致假黄疽弹性体(PXE)的钙化表型以及某些婴儿全身动脉钙化病例,而ENPP1缺陷则会导致婴儿全身动脉钙化。ABCC6 主要在肝脏中表达,这给人的印象是肝脏是 PXE/婴儿全身动脉钙化病理生理学的核心。炎症是 PXE 中钙化的促成因素之一,这表明外周组织的作用比预期的要大。在这项研究中,我们研究了骨髓来源的 ABCC6 是否对 PXE 的钙化有贡献。在 Abcc6-/- 小鼠中,我们观察到多个淋巴结和周围结缔组织中普遍存在矿化现象,而且在 Abcc6-/- 小鼠的钙化组织--振膜中发现了广泛的淋巴管网。此外,我们还在 PXE 患者和小鼠皮肤中发现了淋巴管生成的证据,表明这是一个炎症过程。最后,在Abcc6-/-小鼠体内恢复野生型骨髓可显著减少钙化,这表明仅靠肝脏不足以完全抑制矿化。有证据表明 ABCC6 在淋巴细胞中表达,因此我们认为适应性免疫系统和炎症在很大程度上导致了 PXE/婴儿全身动脉钙化的钙化。
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引用次数: 0
The EGR1–Artemin Axis in Keratinocytes Enhances the Innervation of Epidermal Sensory Neurons during Skin Inflammation Induced by House Dust Mite Extract from Dermatophagoides farinae 角质形成细胞中的 EGR1-ARTN 轴可在 Dermatophagoides farinae 家尘螨提取物诱发皮肤炎症期间增强表皮感觉神经元的神经支配功能
IF 5.7 2区 医学 Q1 DERMATOLOGY Pub Date : 2024-08-01 DOI: 10.1016/j.jid.2024.01.017

Epidermal hyperinnervation is a critical feature of pruritus during skin inflammation. However, the mechanisms underlying epidermal hyperinnervation are unclear. This study investigates the role of the transcription factor EGR1 in epidermal innervation by utilizing wild-type (Egr1+/+) and Egr1-null (Egr1‒/‒) mice topically applied Dermatophagoides farinae extract from dust mite. Our findings revealed that Egr1‒/‒ mice exhibited reduced scratching behaviors and decreased density of epidermal innervation compared with Egr1+/+ mice. Furthermore, we identified artemin, a neurotrophic factor, as an EGR1 target responsible for Dermatophagoides farinae extract–induced hyperinnervation. It has been demonstrated that Dermatophagoides farinae extract stimulates toll-like receptors in keratinocytes. To elucidate the cellular mechanism, we stimulated keratinocytes with Pam3CSK4, a toll-like receptor 1/2 ligand. Pam3CSK4 triggered a toll-like receptor 1/2–mediated signaling cascade involving IRAK4, IκB kinase, MAPKs, ELK1, EGR1, and artemin, leading to increased neurite outgrowth and neuronal migration. In addition, increased expression of EGR1 and artemin was observed in the skin tissues of patients with atopic dermatitis. These findings highlight the significance of the EGR1–artemin axis in keratinocytes, promoting the process of epidermal innervation and suggesting it as a potential therapeutic target for alleviating itch and pain associated with house dust mite–induced skin inflammation.

表皮神经过度支配是皮肤炎症期间瘙痒的一个重要特征。然而,表皮神经过度支配的机制尚不清楚。本研究利用野生型小鼠(Egr1+/+)和 Egr1-null(Egr1-/-)小鼠局部应用 Dermatophagoides farinae(DfE)尘螨提取物,研究转录因子 EGR1 在表皮神经支配中的作用。我们的研究结果表明,与 Egr1+/+ 小鼠相比,Egr1-/- 小鼠的搔抓行为减少,表皮神经支配密度降低。此外,我们还发现神经营养因子青蒿素(ARTN)是导致 DfE 诱导神经支配过度的 EGR1 靶点。已有研究证明,DfE 可刺激角质形成细胞中的类收费受体(TLRs)。为了阐明其细胞机制,我们用收费样受体(TLR)1/2 配体 Pam3CSK4 刺激角质形成细胞。Pam3CSK4 触发了 TLR1/2 介导的信号级联,涉及 IRAK4、IKK、MAPKs、ELK1、EGR1 和 ARTN,导致神经元外生和神经元迁移增加。此外,在特应性皮炎患者的皮肤组织中观察到 EGR1 和 ARTN 的表达增加。这些发现凸显了 EGR1-ARTN 轴在角质形成细胞中的重要性,它促进了表皮神经支配过程,并建议将其作为潜在的治疗靶点,以减轻与屋尘螨诱发的皮肤炎症相关的瘙痒和疼痛。
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引用次数: 0
007 Cytokine profiling in pemphigus vulgaris & alopecia areata reveals analogous genetic underpinning of autoimmune skin disease 007 丘疹性荨麻疹和斑秃中的细胞因子谱分析揭示了自身免疫性皮肤病的类似遗传基础
IF 5.7 2区 医学 Q1 DERMATOLOGY Pub Date : 2024-08-01 DOI: 10.1016/j.jid.2024.06.023
R. Schwartz, K. Seiffert-Sinha, A.A. Sinha
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引用次数: 0
048 Activation of CD1a-autoreactive T cells in acidic microenvironment 048 在酸性微环境中激活 CD1a 自反应 T 细胞
IF 5.7 2区 医学 Q1 DERMATOLOGY Pub Date : 2024-08-01 DOI: 10.1016/j.jid.2024.06.064
I. Karantza, R. Chakravarthy, A. de Jong
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引用次数: 0
032 Non-classical presentation of IL-6 to endothelial cells (ECs) biases the outcome of antigen presentation by Langerhans cells (LCs) to CD4 T cells away from an IFNγ response and toward an IL-17A response 032 IL-6 向内皮细胞(ECs)的非典型呈递使朗格汉斯细胞(LCs)向 CD4 T 细胞呈递抗原的结果偏离 IFNγ 反应,而转向 IL-17A 反应
IF 5.7 2区 医学 Q1 DERMATOLOGY Pub Date : 2024-08-01 DOI: 10.1016/j.jid.2024.06.048
W. Diing, L.L. Stohl, J.A. Wagner, R.D. Granstein
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引用次数: 0
034 Downregulation of Ebp1Khib210 promotes keratinocyte proliferation through induction of TIF-IA-mediated rRNA synthesis 034 下调 Ebp1Khib210 可通过诱导 TIF-IA 介导的 rRNA 合成促进角质形成细胞增殖
IF 5.7 2区 医学 Q1 DERMATOLOGY Pub Date : 2024-08-01 DOI: 10.1016/j.jid.2024.06.050
Y. Wang, J. Li, K. Zhang
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引用次数: 0
期刊
Journal of Investigative Dermatology
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