Rajakulasingam K, Durham S R, O'Brien F, Humbert M, Barata L T, Reece L, Kay A B, Grant J A
Upper Respiratory Medicine, Imperial College of Medicine, National Heart and Lung Institute, London, England.
J Allergy Clin Immunol. 1997 Jul;100(1):78-86. doi: 10.1016/s0091-6749(97)70198-2.
IgE-dependent activation of mast cells and basophils through the high-affinity IgE receptor (Fc epsilon RI) is involved in the pathogenesis of allergen-induced immediate and late responses.
We investigated the expression and cellular distribution of Fc epsilon RI in the nasal mucosa after allergen challenge in patients with summer hay fever.
Fourteen grass pollen-sensitive patients and seven normal control subjects underwent nasal challenge with grass pollen and allergen diluent in random order separated by 2 weeks. Nasal airway caliber was monitored by acoustic rhinometry, and nasal biopsy was performed at 6 hours. Messenger RNA for Fc epsilon RI was determined by using reverse-transcription polymerase chain reaction, and Fc epsilon RI protein expression was determined by immunohistology with a mouse monoclonal antibody (22E7) and a rabbit polyclonal antibody (997) directed against the alpha subunit. Co-localization of Fc epsilon RI receptors was performed by using double-immunostaining methods.
In atopic subjects, there was a significant early decrease in nasal airway caliber, which extended up to 6 hours after allergen challenge. Fc epsilon RI mRNA levels were elevated at 6 hours (p = 0.03). Cells expressing Fc epsilon RI protein were increased in patients with atopic rhinitis compared with normal control subjects (p = 0.03). Further increases in Fc epsilon RI+ cells were observed after allergen challenge only in the atopic group (p = 0.02). Double immunohistochemistry revealed that the majority of Fc epsilon RI+ cells were mast cells (64%), followed by macrophages (20%), eosinophils (4%), and dendritic cells (2%), with 10% Fc epsilon RI+ cells being unidentified.
Our results demonstrate increased Fc epsilon RI expression during allergen-induced rhinitis and highlight a potential target for treatment.
通过高亲和力IgE受体（FcεRI）介导的肥大细胞和嗜碱性粒细胞的IgE依赖性激活参与变应原诱导的速发和迟发反应的发病机制。
我们研究了夏季花粉症患者变应原激发后鼻黏膜中FcεRI的表达及细胞分布。
14名对草花粉敏感的患者和7名正常对照受试者，随机顺序接受草花粉和变应原稀释液的鼻激发，间隔2周。通过声反射鼻测量法监测鼻气道口径，并在6小时时进行鼻活检。采用逆转录聚合酶链反应测定FcεRI的信使核糖核酸，并用针对α亚基的小鼠单克隆抗体（22E7）和兔多克隆抗体（997）通过免疫组织学测定FcεRI蛋白表达。采用双重免疫染色方法进行FcεRI受体的共定位。
在特应性受试者中，鼻气道口径在变应原激发后早期显著减小，可持续至激发后6小时。FcεRI信使核糖核酸水平在6小时时升高（p = 0.03）。与正常对照受试者相比，变应性鼻炎患者中表达FcεRI蛋白的细胞增多（p = 0.03）。仅在特应性组中，变应原激发后FcεRI+细胞进一步增加（p = 0.02）。双重免疫组织化学显示，大多数FcεRI+细胞为肥大细胞（64%），其次为巨噬细胞（20%）、嗜酸性粒细胞（4%）和树突状细胞（2%），10%的FcεRI+细胞未明确。
我们的结果表明变应原诱导的鼻炎期间FcεRI表达增加，并突出了一个潜在的治疗靶点。
