van der Veen M J, Van Neerven R J, De Jong E C, Aalberse R C, Jansen H M, van der Zee J S
Department of Pulmonology, Academic Medical Center, University of Amsterdam, The Netherlands.
Clin Exp Allergy. 1999 Feb;29(2):217-27. doi: 10.1046/j.1365-2222.1999.00466.x.
Increasing insights into the mechanism underlying the allergen-induced late asthmatic response (LAR) have been gained with implication of activated eosinophils and CD4+ T lymphocytes. However, the patient characteristics that indicate the individual capacity to develop a LAR are not well-defined.
In 22 subjects with mild to moderate house dust mite-allergic asthma, we investigated the relationship between the LAR and two other models of late-phase allergic inflammation, i.e. the allergen-specific proliferative response of peripheral blood T lymphocytes in vitro and the late cutaneous response. Non-specific bronchial responsiveness (PC20histamine), lung function (FEV1), peripheral blood eosinophil count, early phase allergic skin sensitivity, and levels of total and specific immunoglobulin E (IgE) were determined prior to bronchial allergen challenge. Serum levels of interleukin-5 (IL-5) were measured before and at several time points after allergen inhalation.
A significant correlation was found between the magnitude of the LAR and the allergen-specific proliferative response of peripheral T lymphocytes (r = 0.44, P = 0.04) but not the late cutaneous response. Stepwise-multiple linear regression of the magnitude of the LAR on the parameters analysed at baseline, resulted in a model combining PC20 histamine, early phase allergic skin sensitivity, and the allergen-specific proliferative response of peripheral T lymphocytes (R2 = 0.84, P<0.001). No contribution of the late cutaneous response to the prediction of the LAR was found. Serum levels of IL-5 increased significantly at 6 h (P = 0.01) and 24 h (P = 0.003) after bronchial allergen challenge and correlated with the allergen-specific proliferative response of peripheral T lymphocytes in vitro (rho = 0.48, P = 0.02).
The findings in this study point to a role of TH2-lymphocyte responses in the development of the allergen-induced LAR. In allergic asthmatic patients, allergen-specific responsiveness of peripheral T-lymphocytes in vitro may serve as a model to determine the individual capacity to develop a LAR after allergen inhalation.
随着活化嗜酸性粒细胞和CD4 + T淋巴细胞的参与，人们对变应原诱导的迟发性哮喘反应（LAR）的潜在机制有了越来越深入的了解。然而，表明个体发生LAR能力的患者特征尚未明确界定。
在22名轻度至中度屋尘螨过敏性哮喘患者中，我们研究了LAR与另外两种迟发性过敏炎症模型之间的关系，即外周血T淋巴细胞在体外的变应原特异性增殖反应和迟发性皮肤反应。在支气管变应原激发前测定非特异性支气管反应性（组胺PC20）、肺功能（FEV1）、外周血嗜酸性粒细胞计数、早期过敏性皮肤敏感性以及总免疫球蛋白E（IgE）和特异性IgE水平。在变应原吸入前和吸入后的几个时间点测量血清白细胞介素-5（IL-5）水平。
发现LAR的程度与外周T淋巴细胞的变应原特异性增殖反应之间存在显著相关性（r = 0.44，P = 0.04），但与迟发性皮肤反应无关。对基线时分析的参数进行逐步多元线性回归，得出一个模型，该模型结合了组胺PC20、早期过敏性皮肤敏感性和外周T淋巴细胞的变应原特异性增殖反应（R2 = 0.84，P<0.001）。未发现迟发性皮肤反应对LAR预测有贡献。支气管变应原激发后6小时（P = 0.01）和24小时（P = 0.003）血清IL-5水平显著升高，并与外周T淋巴细胞在体外的变应原特异性增殖反应相关（rho = 0.48，P = 0.02）。
本研究结果表明TH2淋巴细胞反应在变应原诱导的LAR发生中起作用。在过敏性哮喘患者中，外周T淋巴细胞在体外的变应原特异性反应性可作为确定个体在变应原吸入后发生LAR能力的模型。
