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首页> 外文期刊>Allergy >Mast cells are critically involved in serum-mediated vascular leakage in chronic urticaria beyond high-affinity IgE receptor stimulation.
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Mast cells are critically involved in serum-mediated vascular leakage in chronic urticaria beyond high-affinity IgE receptor stimulation.

机译：在高亲和力IgE受体刺激之外，肥大细胞还参与慢性荨麻疹的血清介导的血管渗漏。

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BACKGROUND: Chronic urticaria (CU) is one of the most common skin disorders whose pathogenic mechanisms are not fully clarified. Autoimmune aetiology can be ascribed to 45% of patients with CU, and basophil histamine release is positive in 40% of cases. Our aim was to use a novel approach to evaluate the serum permeabilizing effect to identify the mediators of endothelial cell (EC) leakage and to define the role of mast cells (MCs) in the process. METHODS: Permeabilizing activity of sera from 19 patients with CU and 11 healthy blood donors was evaluated by measuring serum-induced degranulation of two MC lines, expressing (LAD2) or lacking (HMC-1) the IgE receptor. Mast cell supernatant (SN) was then incubated with an EC monolayer, and endothelial permeability was evaluated by Fluorescein isothiocyanate-bovine serum albumin leakage in a transwell system. RESULTS: All 19 patient sera failed to induce direct EC leakage, but 15/19 and 17/19 promoted degranulation of HMC-1 and LAD2, respectively. Interestingly, 85% of autologous serum skin test-negative sera were able to cause MC degranulation. Also, 17/19 SNs from HMC-1 and all SNs from LAD2 incubated with CU sera increased endothelial permeability. Endothelial cell leakage remained unchanged after Ig depletion and was prevented by antihistamine, platelet-activating factor or leukotriene antagonist. CONCLUSIONS: Our study shows that CU sera are able to degranulate MCs through an IgE- and IgG-independent mechanism. The nature of histamine-releasing factors involved is still unclear, but our finding opens new ways to the understanding of the pathogenesis of CU, particularly in patients not showing circulating autoantibodies to FcepsilonRI or IgE.
机译：背景：慢性荨麻疹（CU）是最常见的皮肤病之一，其致病机理尚未完全阐明。自身免疫病因可归因于CU患者的45％，嗜碱性粒细胞组胺的释放在40％的患者中为阳性。我们的目标是使用一种新方法来评估血清通透性作用，以鉴定内皮细胞（EC）泄漏的介质，并定义肥大细胞（MCs）在此过程中的作用。方法：通过测量血清诱导的表达（LAD2）或缺乏（HMC-1）IgE受体的两条MC系的脱颗粒，评估了19位CU患者和11位健康献血者血清的通透性。然后将肥大细胞上清液（SN）与EC单层孵育，并通过异硫氰酸荧光素-牛血清白蛋白渗漏在Transwell系统中评估内皮通透性。结果：所有19例患者血清均未能诱导直接EC泄漏，但15/19和17/19分别促进了HMC-1和LAD2的脱颗粒。有趣的是，自体血清皮肤测试阴性血清的85％能够引起MC脱颗粒。同样，来自HMC-1的17/19 SN和来自LAD2的所有SN与CU血清一起孵育均会增加内皮通透性。 Ig耗尽后内皮细胞渗漏保持不变，并被抗组胺药，血小板活化因子或白三烯拮抗剂阻止。结论：我们的研究表明，CU血清能够通过IgE和IgG非依赖性机制使MC脱粒。尚不清楚所涉及的组胺释放因子的性质，但我们的发现为了解CU的发病机理开辟了新途径，特别是在未显示FcepsilonRI或IgE循环自身抗体的患者中。

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