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慢性自发性荨麻疹:现有及新型生物制剂。

Chronic Spontaneous Urticaria: Current and Emerging Biologic Agents.

机构信息

Division of Rheumatology, Allergy and Immunology, University of Cincinnati, 234 Goodman Street, Cincinnati, OH 45219, USA.

Department of Allergy and Clinical Immunology, Cleveland Clinic, 9500 Euclid Avenue, A90, Cleveland, OH 44195, USA.

出版信息

Immunol Allergy Clin North Am. 2024 Nov;44(4):595-613. doi: 10.1016/j.iac.2024.07.001. Epub 2024 Aug 26.

Abstract

Antihistamine refractory chronic spontaneous urticaria (CSU) has a prevalence of up to 50%. Anti-immunoglobulin E (IgE) therapies have revolutionized management of CSU, yet refractory cases persist, suggesting a role for biologic agents that impact alternative routes of mast cell stimulation independent of cross-linking at FcεR1. This review addresses anti-IgE and Th2-targeted therapies in the management of CSU. In addition, we explore novel treatments targeting alternative pathways of mast cell activation including MAS-related G protein-coupled receptor-X2 and sialic acid-binding immunoglobulin-like lectin-6, inhibiting intracellular signaling via Bruton's tyrosine kinase, and disrupting KIT activation by SCF.

摘要

抗组胺药难治性慢性自发性荨麻疹(CSU)的患病率高达 50%。抗免疫球蛋白 E(IgE)疗法彻底改变了 CSU 的治疗方法,但仍有难治性病例存在,这表明生物制剂可能在发挥作用,这些生物制剂通过不与 FcεR1 交联而影响肥大细胞刺激的替代途径。这篇综述讨论了抗 IgE 和针对 Th2 的治疗方法在 CSU 治疗中的应用。此外,我们还探讨了针对肥大细胞激活替代途径的新型治疗方法,包括 MAS 相关 G 蛋白偶联受体-X2 和唾液酸结合免疫球蛋白样凝集素-6,通过布鲁顿酪氨酸激酶抑制细胞内信号转导,以及通过 SCF 破坏 KIT 的激活。

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