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“组学”时代银屑病的发病机制。第一部分。流行病学、临床表现、免疫及神经内分泌紊乱

Pathogenesis of psoriasis in the "omic" era. Part I. Epidemiology, clinical manifestation, immunological and neuroendocrine disturbances.

作者信息

Samotij Dominik, Nedoszytko Bogusław, Bartosińska Joanna, Batycka-Baran Aleksandra, Czajkowski Rafał, Dobrucki Iwona T, Dobrucki Lawrence W, Górecka-Sokołowska Magdalena, Janaszak-Jasienicka Anna, Krasowska Dorota, Kalinowski Leszek, Macieja-Stawczyk Marta, Nowicki Roman J, Owczarczyk-Saczonek Agnieszka, Płoska Agata, Purzycka-Bohdan Dorota, Radulska Adrianna, Reszka Edyta, Siekierzycka Anna, Słomiński Andrzej, Słomiński Radomir, Sobalska-Kwapis Marta, Strapagiel Dominik, Szczerkowska-Dobosz Aneta, Szczęch Justyna, Żmijewski Michał, Reich Adam

机构信息

Department of Dermatology, University of Rzeszow, Rzeszow, Poland.

Department of Dermatology, Venereology and Allergology, Medical University of Gdansk, Gdansk, Poland.

出版信息

Postepy Dermatol Alergol. 2020 Apr;37(2):135-153. doi: 10.5114/ada.2020.94832. Epub 2020 May 5.

DOI:
10.5114/ada.2020.94832
PMID:32489346
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7262814/
Abstract

Psoriasis is a common, chronic, inflammatory, immune-mediated skin disease affecting about 2% of the world's population. According to current knowledge, psoriasis is a complex disease that involves various genes and environmental factors, such as stress, injuries, infections and certain medications. The chronic inflammation of psoriasis lesions develops upon epidermal infiltration, activation, and expansion of type 1 and type 17 Th cells. Despite the enormous progress in understanding the mechanisms that cause psoriasis, the target cells and antigens that drive pathogenic T cell responses in psoriatic lesions are still unproven and the autoimmune basis of psoriasis still remains hypothetical. However, since the identification of the Th17 cell subset, the IL-23/Th17 immune axis has been considered a key driver of psoriatic inflammation, which has led to the development of biologic agents that target crucial elements of this pathway. Here we present the current understanding of various aspects in psoriasis pathogenesis.

摘要

银屑病是一种常见的慢性炎症性免疫介导性皮肤病,影响着全球约2%的人口。根据目前的认知,银屑病是一种复杂的疾病,涉及多种基因和环境因素,如压力、损伤、感染和某些药物。银屑病皮损的慢性炎症是在1型和17型辅助性T细胞的表皮浸润、激活和扩增后发生的。尽管在理解引发银屑病的机制方面取得了巨大进展,但驱动银屑病皮损中致病性T细胞反应的靶细胞和抗原仍未得到证实,银屑病的自身免疫基础仍然是假设性的。然而,自从发现辅助性T细胞17亚群以来,白细胞介素-23/辅助性T细胞17免疫轴被认为是银屑病炎症的关键驱动因素,这促使了针对该途径关键要素的生物制剂的研发。在此,我们阐述了目前对银屑病发病机制各个方面的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2490/7262814/aa6caee2cdfb/PDIA-37-40509-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2490/7262814/aa6caee2cdfb/PDIA-37-40509-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2490/7262814/aa6caee2cdfb/PDIA-37-40509-g001.jpg

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IL-23 induces regulatory T cell plasticity with implications for inflammatory skin diseases.IL-23 诱导调节性 T 细胞可塑性,对炎症性皮肤病有影响。
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