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特应性皮炎中的炎性小体通路:对炎症机制和治疗靶点的见解

Inflammasome pathways in atopic dermatitis: insights into inflammatory mechanisms and therapeutic targets.

作者信息

Ramos Yasmim Álefe Leuzzi, Pietrobon Anna Julia, Teixeira Franciane Mouradian Emidio, Aoki Valeria, Sato Maria Notomi, Orfali Raquel Leão

机构信息

Department of Dermatology, Laboratório de Investigação Médica em Dermatologia e Imunodeficiências (LIM56), Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brazil.

Department of Dermatology, Laboratório de Investigação Médica em Dermatologia e Imunodeficiências (LIM56), Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brazil.

出版信息

An Bras Dermatol. 2025 Jun 23;100(4):501136. doi: 10.1016/j.abd.2025.501136.

DOI:10.1016/j.abd.2025.501136
PMID:40555102
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12226124/
Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by a complex interaction between genetic, immunological, and environmental factors. The combination of immune dysregulation and skin barrier dysfunction plays a crucial role in the pathogenesis of the disease. The inflammasome, an important intracellular complex of pattern recognition receptors (PRRs), plays a crucial role in the cutaneous inflammatory response, activating caspase-1 and promoting the release of pro-inflammatory cytokines such as interleukin (IL)-1β and IL-18. The role of inflammasome components in regulating the inflammatory response in AD highlights how the activation of these complexes exacerbates inflammation and contributes to the worsening of the disease and tissue damage. The review included observational and experimental studies investigating inflammasome activation in AD and other inflammatory skin diseases. The main mechanisms of inflammasome activation and their impact on the inflammatory environment and skin barrier integrity were discussed. Understanding the role of the inflammasome in AD is essential for the development of new therapeutic approaches aimed at both modulating the immune response and restoring the skin barrier, improving more effective clinical management and patients' quality of life.

摘要

特应性皮炎(AD)是一种慢性炎症性皮肤病,其特征是遗传、免疫和环境因素之间存在复杂的相互作用。免疫失调和皮肤屏障功能障碍的结合在该疾病的发病机制中起着关键作用。炎性小体是模式识别受体(PRR)的一种重要细胞内复合物,在皮肤炎症反应中起关键作用,激活半胱天冬酶-1并促进促炎细胞因子如白细胞介素(IL)-1β和IL-18的释放。炎性小体成分在调节AD炎症反应中的作用突出了这些复合物的激活如何加剧炎症并导致疾病恶化和组织损伤。该综述包括观察性和实验性研究,调查了AD和其他炎症性皮肤病中炎性小体的激活情况。讨论了炎性小体激活的主要机制及其对炎症环境和皮肤屏障完整性的影响。了解炎性小体在AD中的作用对于开发旨在调节免疫反应和恢复皮肤屏障的新治疗方法至关重要,有助于改善更有效的临床管理和患者的生活质量。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e74/12226124/042d8b6df941/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e74/12226124/b957ef4f9f7f/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e74/12226124/2e49efed7839/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e74/12226124/f6da1a960a4e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e74/12226124/042d8b6df941/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e74/12226124/b957ef4f9f7f/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e74/12226124/2e49efed7839/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e74/12226124/f6da1a960a4e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e74/12226124/042d8b6df941/gr4.jpg

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本文引用的文献

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Inflammasome components as new therapeutic targets in inflammatory disease.炎症小体成分作为炎症性疾病的新治疗靶点。
Nat Rev Immunol. 2025 Jan;25(1):22-41. doi: 10.1038/s41577-024-01075-9. Epub 2024 Sep 9.
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Cutaneous inflammasome driving ASC / gasdermin-D activation and IL-1β-secreting macrophages in severe atopic dermatitis.
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Gasdermin D (GSDMD) Is Upregulated in Psoriatic Skin-A New Potential Link in the Pathogenesis of Psoriasis.Gasdermin D(GSDMD)在银屑病皮肤中上调——银屑病发病机制中的一个新的潜在关联。
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