Expression of Tissue Factor by Eosinophils in Patients with Chronic Urticaria
Expression of Tissue Factor by Eosinophils in Patients with Chronic Urticaria
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DOI：
10.1159/000155748
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发表时间：
2009-01-01
影响因子：
2.8
通讯作者：
Asero, Riccardo
中科院分区：
文献类型：
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作者：
Cugno, Massimo;Marzano, Angelo V.;Asero, Riccardo
背景资料：尽管目前认为几例慢性荨麻疹（CU）是自身免疫性的，与组胺释放自身抗体有关，但已描述了通过组织因子（TF）激活血液凝固和TF在病变皮肤中的强烈表达。嗜酸性粒细胞，这是涉及CU皮肤病变，最近被证明是TF在人类血液中的主要来源。我们评估了嗜酸性粒细胞是否是CU皮损中TF的细胞来源。方法：对20例重症CU患者进行回顾性分析。皮肤活检标本取自风团。对照组由不同类型皮肤肿瘤（10）和各种非嗜酸性浸润性皮肤疾病（包括白细胞破碎性血管炎（7）、扁平苔藓（8）和肥大细胞增多症（3））的病灶周围正常皮肤标本组成。TF表达通过免疫组织化学方法使用抗TF单克隆抗体进行评价。共定位TF和嗜酸性粒细胞阳离子蛋白，嗜酸性粒细胞的一个经典的细胞标志物，通过双染色研究，使用2种特异性单克隆抗体在4个标本显示最高的TF反应性评分。结果如下：CU患者的所有标本均明确显示TF表达，而在所有正常对照标本（p = 0.0001）和非嗜酸性粒细胞浸润的皮肤疾病（p = 0.001-0.0001）中均不存在TF表达。TF和嗜酸性粒细胞阳离子蛋白的双染实验清楚地表明TF阳性细胞为嗜酸性粒细胞。结论：嗜酸性粒细胞是CU皮损TF的主要来源。这一发现强调了这些细胞在CU病理生理学中的作用，并可能为新的治疗策略铺平道路。版权所有（C）2008 S. Karger AG，巴塞尔
Background: Although several cases of chronic urticaria (CU) are currently regarded as autoimmune in origin, associated with histamine-releasing autoantibodies, an activation of blood coagulation via tissue factor (TF) and a strong expression of TF in lesional skin have been described. Eosinophils, which are involved in CU skin lesions, have recently been demonstrated as the major source of TF in human blood. We assessed whether eosinophils are the cellular source of TF in CU skin lesions. Methods: Twenty patients with severe CU were studied. Skin biopsy specimens were taken from wheals. The control group consisted of specimens of perilesional normal skin from different types of skin tumours (10) and various skin disorders with non-eosinophilic infiltrates, including leukocytoclastic vasculitis (7), lichen planus (8) and mastocytosis (3). TF expression was evaluated by immunohistochemical methods using an anti-TF monoclonal antibody. Co-localization of TF and eosinophil cationic protein, a classic cell marker of eosinophils, was investigated by double-staining studies using 2 specific monoclonal antibodies in the 4 specimens showing the highest TF reactivity scores. Results: All specimens from patients with CU clearly showed TF expression that was absent in all normal control specimens (p = 0.0001) and in the skin disorders with non-eosinophilic infiltrates (p = 0.001-0.0001). The double-staining experiments for TF and eosinophil cationic protein clearly showed that the TF-positive cells were eosinophils. Conclusions: Eosinophils are the main source of TF in CU lesional skin. This finding highlights the role of these cells in the pathophysiology of CU and might pave the way for new therapeutic strategies. Copyright (C) 2008 S. Karger AG, Basel