Tanaka N, Watanabe J, Kitamura T, Yamada Y, Kanegasaki S, Nakata K
Laboratory of Culture Collection, The Institute of Medical Science, The University of Tokyo, Japan.
FEBS Lett. 1999 Jan 15;442(2-3):246-50. doi: 10.1016/s0014-5793(98)01668-8.
Mice deficient in granulocyte-macrophage colony stimulating factor (GM-CSF) develop pulmonary alveolar proteinosis (PAP). We found that bronchoalveolar lavage fluid (BALF) from 11 patients with idiopathic pulmonary alveolar proteinosis (IPAP) suppressed the growth of peripheral blood monocytes and TF-1 cells, a cell line dependent on either GM-CSF or interleukin-3 (IL-3). The inhibitory effect of PAP-BALF occurred only when TF-1 cells were cultured with GM-CSF but not when cultured with IL-3, suggesting that PAP-BALF contains a factor that specifically interferes with GM-CSF function. 125I-GM-CSF binding to TF-1 cells was prevented in the presence of BALF from IPAP patients. Furthermore, cross-linking of 125I-GM-CSF to IPAP-BALF produced two major bands on SDS-PAGE; these bands were not observed in normal BALF. These data suggest that IPAP is caused by expression of binding factor(s) which inhibit GM-CSF function in the lung.
粒细胞-巨噬细胞集落刺激因子（GM-CSF）缺乏的小鼠会发生肺泡蛋白沉积症（PAP）。我们发现，11例特发性肺泡蛋白沉积症（IPAP）患者的支气管肺泡灌洗液（BALF）抑制外周血单核细胞和TF-1细胞的生长，TF-1细胞是一种依赖GM-CSF或白细胞介素-3（IL-3）的细胞系。PAP-BALF的抑制作用仅在TF-1细胞与GM-CSF共同培养时出现，而与IL-3共同培养时则不出现，这表明PAP-BALF含有一种特异性干扰GM-CSF功能的因子。在IPAP患者的BALF存在的情况下，125I-GM-CSF与TF-1细胞的结合受到抑制。此外，125I-GM-CSF与IPAP-BALF的交联在SDS-PAGE上产生了两条主要条带；在正常BALF中未观察到这些条带。这些数据表明，IPAP是由肺中抑制GM-CSF功能的结合因子的表达引起的。
