Robinson D S, Tsicopoulos A, Meng Q, Durham S, Kay A B, Hamid Q
National Heart and Lung Institute, London, United Kingdom.
Am J Respir Cell Mol Biol. 1996 Feb;14(2):113-7. doi: 10.1165/ajrcmb.14.2.8630259.
Interleukin-10 (IL-10) inhibits T-lymphocyte proliferation and production of cytokines. We have examined expression of IL-10 messenger RNA (mRNA) in atopic asthma and in allergen and tuberculin skin responses by in situ hybridization. The proportion of bronchoalveolar lavage (BAL) cells positive for IL-10 mRNA was increased in a group of 10 symptomatic asthmatics when compared with control subjects (17.5% versus 5.2% BAL cells positive; P < 0.001). In a separate group of six mild atopic asthmatics, there was an increased proportion of BAL cells positive for IL-10 mRNA 24 h after allergen inhalation challenge compared with diluent challenge BAL from the same subjects (24% versus 10%; P < 0.005). By simultaneous in situ hybridization and immunocytochemistry, IL-10 mRNA was localized to both CD3+ T cells and CD68+ alveolar macrophages in BAL, with a significantly more prominent T-cell signal in the symptomatic asthmatics compared with control subjects and after allergen challenge compared with diluent challenge of the mild asthmatic subjects. It has been suggested that IL-10 production is a late event after T-cell activation. To examine kinetics and specificity of IL-10 mRNA expression, skin biopsies were obtained from atopic, tuberculin-sensitive subjects at 1, 6, and 48 h after cutaneous injection of allergen or tuberculin. With both stimuli, there was an increase in IL-10 mRNA-positive cells at 6 h when compared with control sites injected with appropriate diluent which were biopsied 24 h after injection (P < 0.01 for allergen and P < 0.02 for tuberculin). These findings are compatible with the hypothesis that IL-10 mRNA is expressed in both macrophages and T lymphocytes in the airway in asthma and that IL-10 mRNA expression is induced from T lymphocytes in response to allergen. This response may also occur in other types of cell-mediated inflammation.
白细胞介素-10（IL-10）可抑制T淋巴细胞增殖及细胞因子的产生。我们通过原位杂交技术检测了特应性哮喘以及变应原和结核菌素皮肤反应中IL-10信使核糖核酸（mRNA）的表达情况。与对照组相比，10名有症状哮喘患者支气管肺泡灌洗（BAL）细胞中IL-10 mRNA阳性比例升高（BAL细胞阳性比例分别为17.5%和5.2%；P<0.001）。在另一组6名轻度特应性哮喘患者中，变应原吸入激发后24小时，BAL细胞中IL-10 mRNA阳性比例高于同一患者用稀释剂激发后的BAL（分别为24%和10%；P<0.005）。通过同时进行原位杂交和免疫细胞化学检测，发现BAL中IL-10 mRNA定位于CD3+T细胞和CD68+肺泡巨噬细胞，与对照组相比，有症状哮喘患者的T细胞信号明显更突出，与轻度哮喘患者用稀释剂激发相比，变应原激发后的T细胞信号更突出。有人提出IL-10的产生是T细胞激活后的晚期事件。为了研究IL-10 mRNA表达的动力学和特异性，在特应性、结核菌素敏感的受试者皮肤注射变应原或结核菌素后1、6和48小时获取皮肤活检标本。两种刺激下，与注射适当稀释剂后24小时活检的对照部位相比，6小时时IL-10 mRNA阳性细胞均增加（变应原刺激P<0.01，结核菌素刺激P<0.02）。这些发现与以下假设相符：哮喘气道中的巨噬细胞和T淋巴细胞均表达IL-10 mRNA，且变应原可诱导T淋巴细胞表达IL-10 mRNA。这种反应也可能发生在其他类型的细胞介导的炎症中。
