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慢性自发性荨麻疹:自身免疫作用的新证据。

Chronic spontaneous urticaria: new evidences on the role of autoimmunity.

机构信息

Institute of Allergology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin.

Fraunhofer Institute for Translational Medicine and Pharmacology ITMP, Allergology and Immunology, Berlin, Germany.

出版信息

Curr Opin Allergy Clin Immunol. 2023 Oct 1;23(5):438-445. doi: 10.1097/ACI.0000000000000927. Epub 2023 Jul 6.

DOI:10.1097/ACI.0000000000000927
PMID:37459281
Abstract

PURPOSE OF REVIEW

The purpose of this review is to provide an overview of the recent advancements and relevance of the autoimmune theories in chronic spontaneous urticaria (CSU).

RECENT FINDINGS

Two primary types of autoimmunity, Type I and Type IIb, have emerged as major contributors to CSU, characterized by immunoglobulin E (IgE) and immunoglobulin G (IgG) autoantibodies, respectively. Genetic evidence supports the notion that CSU shares more similarities with other autoimmune diseases rather than atopic diseases. Novel autoallergens such as FcεRI and tissue transglutaminase have been identified, contributed to our understanding of autoimmune mechanisms. Furthermore, the potential overlap between Type I and Type IIb autoimmunity has been recognized. Evaluating the autoimmune status of CSU patients through biomarkers and understanding their clinical implications is vital for effective management. For instance, CSU patients with Type IIb autoimmunity, with or without coexisting Type I autoimmunity, may exhibit resistance to H1-antihistamines and omalizumab treatment but could potentially respond well to cyclosporine or Bruton's tyrosine kinase inhibitors.

SUMMARY

Further investigations are needed to explore new autoallergens and autoantibodies in CSU, establishing their connection to the development of autoimmunity. The efficacy of novel drugs targeting different mechanisms should be examined to determine their responses in both autoimmune CSU and nonautoimmunity-related CSU.

摘要

目的综述

本文旨在概述自身免疫理论在慢性自发性荨麻疹(CSU)中的最新进展及其相关性。

最新发现

两种主要的自身免疫类型,即 I 型和 IIb 型,已成为 CSU 的主要致病因素,分别表现为免疫球蛋白 E(IgE)和免疫球蛋白 G(IgG)自身抗体。遗传证据支持这样一种观点,即 CSU 与其他自身免疫性疾病而非特应性疾病具有更多的相似性。新型自身抗原,如 FcεRI 和组织转谷氨酰胺酶已被鉴定出来,有助于我们理解自身免疫机制。此外,I 型和 IIb 型自身免疫之间的潜在重叠已被认识到。通过生物标志物评估 CSU 患者的自身免疫状态并了解其临床意义对于有效管理至关重要。例如,具有 IIb 型自身免疫的 CSU 患者,无论是否存在共存的 I 型自身免疫,可能对 H1 抗组胺药和奥马珠单抗治疗产生耐药性,但可能对环孢素或布鲁顿酪氨酸激酶抑制剂反应良好。

总结

需要进一步研究来探索 CSU 中的新型自身抗原和自身抗体,并确定它们与自身免疫发展的关系。应检查针对不同机制的新型药物的疗效,以确定它们在自身免疫性 CSU 和非自身免疫相关 CSU 中的反应。

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