Yamaguchi E, Okazaki N, Tsuneta Y, Abe S, Terai T, Kawakami Y
First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
Am Rev Respir Dis. 1988 Sep;138(3):645-51. doi: 10.1164/ajrccm/138.3.645.
To investigate whether interleukins are involved in the formation of alveolitis in pulmonary sarcoidosis, interleukin-1 (IL-1) production by LPS-stimulated alveolar macrophages (AM) and interleukin-2 (IL-2) production by PHA-stimulated lung and blood T-cells were determined in 35 untreated patients with pulmonary sarcoidosis. The amount of IL-1 produced by AM (BAL IL-1) was significantly increased in patients with pulmonary sarcoidosis compared with that in 18 control subjects. BAL IL-1 showed a significant positive correlation with the intensity of alveolitis assessed by the proportion of lymphocytes in bronchoalveolar lavage fluid (BALF) and the absolute number of lymphocytes per milliliter of BALF. However, the amount of IL-2 produced by lung T-cells (BALT IL-2) showed a significant negative correlation with the intensity of alveolitis. BALT IL-2 was significantly lower than the amount of IL-2 produced by blood T-cells (PBT IL-2). There was no correlation between PBT IL-2 and the intensity of alveolitis. These results suggest that IL-2 contributes to the formation and maintenance of alveolitis in pulmonary sarcoidosis, whereas IL-2 production by lung T-cells is suppressed to down-regulate the enhanced immune processes at the site of disease. The possibility that this hyporesponsiveness of lung T-cells to PHA has resulted from the modulation of the T3-T cell receptor complex remains to be determined.
为了研究白细胞介素是否参与结节病肺泡炎的形成,我们测定了35例未经治疗的结节病患者经脂多糖(LPS)刺激的肺泡巨噬细胞(AM)产生白细胞介素-1(IL-1)以及经PHA刺激的肺和血液T细胞产生白细胞介素-2(IL-2)的情况。与18名对照受试者相比,结节病患者AM产生的IL-1量(支气管肺泡灌洗IL-1)显著增加。支气管肺泡灌洗IL-1与通过支气管肺泡灌洗液(BALF)中淋巴细胞比例和每毫升BALF中淋巴细胞绝对数评估的肺泡炎强度呈显著正相关。然而,肺T细胞产生的IL-2量(支气管肺泡灌洗T细胞IL-2)与肺泡炎强度呈显著负相关。支气管肺泡灌洗T细胞IL-2显著低于血液T细胞产生的IL-2量(外周血T细胞IL-2)。外周血T细胞IL-2与肺泡炎强度之间无相关性。这些结果表明,IL-1促成结节病肺泡炎的形成和维持,而肺T细胞产生IL-2受到抑制,以下调疾病部位增强的免疫过程。肺T细胞对PHA反应性降低是否由T3-T细胞受体复合物的调节所致,仍有待确定。