Nagata M, Shibasaki M, Sakamoto Y, Fukuda T, Makino S, Yamamoto K, Dohi Y
Second Department of Internal Medicine, Saitama Medical School, Japan.
J Allergy Clin Immunol. 1994 Aug;94(2 Pt 1):160-6. doi: 10.1016/0091-6749(94)90035-3.
The efficacy of specific immunotherapy has been verified. There is accumulating evidence focusing on the T lymphocyte-eosinophil interaction in the pathogenesis of asthma. The aim of this study was to clarify whether immunotherapy affects the production of eosinophil chemotactic activity (ECA) from peripheral blood mononuclear cells (PBMC).
PBMC obtained from persons with bronchial asthma who were sensitive to Dermatophagoides farinae (Df) or from healthy volunteers were cultured for 96 hours in the presence or absence of Df. ECA in culture supernatants was assayed by means of the modified Boyden's chamber method.
There was no significant difference in the baseline levels of ECA between asthmatic persons treated with immunotherapy and those without immunotherapy. The addition of Df (10 to 10(4) ng/ml) enhanced the ECA production in a dose-dependent fashion in asthmatic persons without immunotherapy, and there was a statistically significant correlation between the concentrations of Df and the levels of ECA (rk = 0.34; p < 0.05). In contrast, Df-dependent ECA production was suppressed in asthmatic persons with immunotherapy, and the suppressive effect was observed from 4 weeks after rush immunotherapy.
These results indicate that immunotherapy induces the suppression of antigen-dependent production of ECA from PBMC. This may contribute to the attenuation of eosinophil infiltration into the airways in asthma patients.
特异性免疫疗法的疗效已得到证实。越来越多的证据聚焦于哮喘发病机制中T淋巴细胞与嗜酸性粒细胞的相互作用。本研究的目的是阐明免疫疗法是否会影响外周血单个核细胞（PBMC）产生嗜酸性粒细胞趋化活性（ECA）。
从对粉尘螨（Df）敏感的支气管哮喘患者或健康志愿者中获取PBMC，在有或无Df存在的情况下培养96小时。采用改良的Boyden小室法检测培养上清液中的ECA。
接受免疫疗法的哮喘患者与未接受免疫疗法的哮喘患者在ECA的基线水平上无显著差异。在未接受免疫疗法的哮喘患者中，添加Df（10至10⁴ ng/ml）以剂量依赖方式增强了ECA的产生，并且Df浓度与ECA水平之间存在统计学显著相关性（rk = 0.34；p < 0.05）。相比之下，接受免疫疗法的哮喘患者中Df依赖的ECA产生受到抑制，且在快速免疫疗法后4周观察到抑制作用。
这些结果表明免疫疗法可诱导抑制PBMC中抗原依赖性ECA的产生。这可能有助于减轻哮喘患者气道中嗜酸性粒细胞的浸润。
