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[嗜酸性粒细胞在特应性皮炎/神经性皮炎发病机制中的作用。嗜酸性粒细胞产物作为疾病活动的标志物]

[The role of eosinophilic granulocytes for the pathogenesis of atopic dermatitis /neurodermatitis. Eosinophilic products as markers of disease activity].

作者信息

Kapp A

机构信息

Funktionsbereich Allergologie und Immundiagnostik, Albert-Ludwigs-Universität Freiburg.

出版信息

Hautarzt. 1993 Jul;44(7):432-6.

PMID:8365876
Abstract

Recent data provide increasing evidence for an immunological basis of atopic dermatitis (AD). Atopyspecific helper T cells (Th2-like T cells) may play a pathogenic role by producing and releasing cytokines that are relevant for the allergic inflammation, such as IL-4, IL-5 and other growth factors. It is suggested that eosinophils play a major role as effector cells mediating the pathogenetically important late-phase reaction, which is associated with significant destruction of the surrounding tissue. Accordingly, a significant preactivation of peripheral blood eosinophils was detected in AD patients, leading to enhanced susceptibility of these cells to distinct stimuli, such as IL-5. Toxic proteins, such as eosinophil cationic protein (ECP), which are contained in the matrix and the core of secondary granules of eosinophils, may play an important role by propagating the allergic inflammatory process and by exerting their direct immunomodulatory effects. A pathogenic role of eosinophils in AD is further supported by the detection of these proteins in eczematous skin of the patients. Furthermore, recent data indicate a significant correlation between disease activity and deposition of eosinophil granule content: ECP serum levels were significantly increased in AD patients. In addition, ECP levels correlated with the disease activity. Moreover, clinical improvement was associated with a decrease both in the clinical score and in serum ECP levels. These data clearly indicate that activated eosinophils are involved in the allergic inflammatory process in AD. Therefore, modulation of eosinophil activation could be an important pharmacologic modality for the treatment of AD in the future.

摘要

近期数据越来越多地证明了特应性皮炎(AD)存在免疫学基础。特应性特异性辅助性T细胞(类Th2 T细胞)可能通过产生和释放与过敏性炎症相关的细胞因子,如白细胞介素-4(IL-4)、白细胞介素-5(IL-5)和其他生长因子,而发挥致病作用。有研究表明,嗜酸性粒细胞作为效应细胞在介导具有重要致病意义的迟发性反应中起主要作用,该反应与周围组织的显著破坏有关。因此,在AD患者中检测到外周血嗜酸性粒细胞有明显的预激活现象,导致这些细胞对不同刺激(如IL-5)的敏感性增强。嗜酸性粒细胞次级颗粒的基质和核心中所含的毒性蛋白,如嗜酸性粒细胞阳离子蛋白(ECP),可能通过促进过敏性炎症过程并发挥其直接的免疫调节作用而发挥重要作用。在患者的湿疹皮肤中检测到这些蛋白,进一步支持了嗜酸性粒细胞在AD中的致病作用。此外,近期数据表明疾病活动度与嗜酸性粒细胞颗粒内容物的沉积之间存在显著相关性:AD患者的ECP血清水平显著升高。此外,ECP水平与疾病活动度相关。而且,临床改善与临床评分和血清ECP水平的降低均有关。这些数据清楚地表明,活化的嗜酸性粒细胞参与了AD的过敏性炎症过程。因此,调节嗜酸性粒细胞的活化可能是未来治疗AD的一种重要药物治疗方式。

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