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Front Immunol. 2022 Jul 28;13:901851. doi: 10.3389/fimmu.2022.901851. eCollection 2022.
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Integrative lipidomic features identify plasma lipid signatures in chronic urticaria.整合脂质组学特征可识别慢性荨麻疹患者的血浆脂质特征。
Front Immunol. 2022 Jul 28;13:933312. doi: 10.3389/fimmu.2022.933312. eCollection 2022.
3
Impaired sweating in patients with cholinergic urticaria is linked to low expression of acetylcholine receptor CHRM3 and acetylcholine esterase in sweat glands.胆碱能性荨麻疹患者的出汗功能障碍与汗腺中乙酰胆碱受体 CHRM3 和乙酰胆碱酯酶表达降低有关。
Front Immunol. 2022 Jul 29;13:955161. doi: 10.3389/fimmu.2022.955161. eCollection 2022.
4
GWAS of Chronic Spontaneous Urticaria Reveals Genetic Overlap with Autoimmune Diseases, Not Atopic Diseases.慢性自发性荨麻疹全基因组关联研究显示其与自身免疫性疾病相关,而与特应性疾病无关。
J Invest Dermatol. 2023 Jan;143(1):67-77.e15. doi: 10.1016/j.jid.2022.07.012. Epub 2022 Aug 4.
5
Identification of Immune Cell-Types and Pathways Involved in Chronic Spontaneous Urticaria.慢性自发性荨麻疹中涉及的免疫细胞类型和途径的鉴定
Front Med (Lausanne). 2022 Jul 7;9:926753. doi: 10.3389/fmed.2022.926753. eCollection 2022.
6
Regulatory T cells and immunoglobulin E: A new therapeutic link for autoimmunity?调节性 T 细胞与免疫球蛋白 E:自身免疫的新治疗靶点?
Allergy. 2022 Nov;77(11):3293-3308. doi: 10.1111/all.15449. Epub 2022 Jul 27.
7
The Role of Crosstalk of Immune Cells in Pathogenesis of Chronic Spontaneous Urticaria.免疫细胞串扰在慢性自发性荨麻疹发病机制中的作用。
Front Immunol. 2022 May 31;13:879754. doi: 10.3389/fimmu.2022.879754. eCollection 2022.
8
Plasma-Derived Exosomes in Chronic Spontaneous Urticaria Induce the Production of Mediators by Human Mast Cells.慢性自发性荨麻疹患者血浆衍生的外泌体诱导人肥大细胞产生介质。
J Invest Dermatol. 2022 Nov;142(11):2998-3008.e5. doi: 10.1016/j.jid.2022.03.037. Epub 2022 Jun 2.
9
Dynamin-related protein 1 differentially regulates FcεRI- and substance P-induced mast cell activation.动力蛋白相关蛋白 1 差异调节 FcεRI 和 P 物质诱导的肥大细胞活化。
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Prevalence and risk factors of chronic urticaria in China: A nationwide cross-sectional study.中国慢性荨麻疹的患病率及危险因素:一项全国性横断面研究。
Allergy. 2022 Jul;77(7):2233-2236. doi: 10.1111/all.15287. Epub 2022 Mar 28.

慢性荨麻疹发病机制的研究进展

Research progress in the pathogenesis of chronic urticaria.

作者信息

Wang Jiayi, Li Jie

机构信息

Department of Dermatology, Xiangya Hospital, Central South University, Changsha 410008.

Hunan Key Laboratory of Skin Cancer and Psoriasis, Xiangya Hospital, Central South University, Changsha 410008.

出版信息

Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2023 Oct 28;48(10):1602-1610. doi: 10.11817/j.issn.1672-7347.2023.230037.

DOI:10.11817/j.issn.1672-7347.2023.230037
PMID:38432889
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10929888/
Abstract

Chronic urticaria is very common in clinic, but its pathogenesis is not fully elucidated. Most patients can't find the exact cause, resulting in misdiagnosis or delayed treatment. Previous studies have found that mast cell activation is the central link in the pathogenesis of chronic urticaria. Genetics, autoimmune, coagulation disorders, and infection may also be involved in the pathophysiological process of chronic urticaria. With the deepening of research, more immune and non-immune mechanisms have been gradually revealed in the pathogenesis of chronic urticaria, such as the interaction of immune cells in the microenvironment of urticaria, intestinal flora and metabolism, neuroimmunity, environmental factors and hormones. Clarifying the pathogenesis of chronic urticaria will help to find more treatment targets and provide more diversified ideas for clinical diagnosis and treatment.

摘要

慢性荨麻疹在临床上非常常见,但其发病机制尚未完全阐明。大多数患者无法找到确切病因,导致误诊或治疗延误。既往研究发现,肥大细胞活化是慢性荨麻疹发病机制的中心环节。遗传、自身免疫、凝血障碍及感染也可能参与慢性荨麻疹的病理生理过程。随着研究的深入,慢性荨麻疹发病机制中逐渐揭示出更多免疫和非免疫机制,如荨麻疹微环境中免疫细胞的相互作用、肠道菌群与代谢、神经免疫、环境因素及激素等。阐明慢性荨麻疹的发病机制将有助于找到更多治疗靶点,为临床诊断和治疗提供更多样化的思路。