Characterization of mononuclear phagocyte subpopulations in the human lung by using monoclonal antibodies: changes in alveolar macrophage phenotype associated with pulmonary sarcoidosis.
Characterization of mononuclear phagocyte subpopulations in the human lung by using monoclonal antibodies: changes in alveolar macrophage phenotype associated with pulmonary sarcoidosis.
复制标题
使用单克隆抗体表征人肺中的单核吞噬细胞亚群：与肺结节病相关的肺泡巨噬细胞表型的变化。
作者：
A. Hance;S. Douches;R. Winchester;V. Ferrans;R. Crystal
目前肺结节病的概念表明，肺泡巨噬细胞在该疾病的发病机制中发挥着核心作用。为了帮助定义结节病中的肺泡巨噬细胞群，我们使用检测单核细胞/巨噬细胞谱系细胞表面抗原的单克隆抗体（63D3、OKM1、M phi P-9、M phi S-1、61D3 和 M phi S-39）比较了结节病患者和正常个体的肺泡巨噬细胞的表面表型。尽管几乎所有血液单核细胞都表达这些抗体检测到的表面抗原，但只有少数正常肺泡巨噬细胞表达相同的表面抗原（每次比较，p 小于 0.05）。然而，在结节病中，表达这些表面抗原的肺泡巨噬细胞的百分比增加（每次与正常肺泡巨噬细胞比较，p 小于 0.05）。一些研究结果支持这样的结论：结节病肺泡巨噬细胞上这些单核细胞谱系表面抗原的表达增加是由于结节病中单核细胞向肺部募集的增加，而不是由于肺泡巨噬细胞的异常“激活”。首先，表达这些抗原的肺泡巨噬细胞具有不成熟的形态。其次，在存在免疫和炎症介质（包括已知结节病肺部存在的介质）的情况下体外培养血液单核细胞和肺泡巨噬细胞，并不能阻止单核细胞单核细胞谱系表面抗原表达的丧失，也不能诱导肺泡巨噬细胞上单核细胞谱系表面抗原的重新表达。第三，单核细胞谱系表面抗原的表达仅在下呼吸道含有数量增加的T淋巴细胞（已知在结节病中释放单核细胞趋化因子的细胞）的患者的结节巨噬细胞上增加。与皮质类固醇通常抑制活动性结节病肺泡炎的知识相一致，当在治疗前和治疗期间评估肺泡巨噬细胞表面抗原的表达时，表达单核细胞谱系表面抗原的肺泡巨噬细胞的百分比在治疗1至3个月后恢复正常。（摘要截断为400字）
Current concepts of pulmonary sarcoidosis suggest that the alveolar macrophage plays a central role in the pathogenesis of the disease. To help define the population of alveolar macrophages in sarcoidosis, we compared the surface phenotype of alveolar macrophages from patients with sarcoidosis and from normal individuals by using monoclonal antibodies (63D3, OKM1, M phi P-9, M phi S-1, 61D3, and M phi S-39) that detect surface antigens on cells of monocyte/macrophage lineage. Although almost all blood monocytes expressed surface antigens detected by each of these antibodies, only a minority of normal alveolar macrophages expressed the same surface antigens (p less than 0.05, each comparison). However, in sarcoidosis, the percentage of alveolar macrophages expressing these surface antigens was increased (p less than 0.05, each comparison with normal alveolar macrophages). Several findings supported the conclusion that the increased expression of these monocyte-lineage surface antigens on sarcoid alveolar macrophages resulted from increased recruitment of monocytes to the lung in sarcoidosis and not from abnormal "activation" of alveolar macrophages. First, alveolar macrophages expressing these antigens had an immature morphology. Second, in vitro cultivation of blood monocytes and alveolar macrophages in the presence of immune and inflammatory mediators, including mediators known to be present in the lung in sarcoidosis, did not prevent the loss of expression of monocyte-lineage surface antigens from monocytes or induce reexpression of monocyte-lineage surface antigens on alveolar macrophages. Third, the expression of monocyte-lineage surface antigens was only increased on sarcoid macrophages from patients whose lower respiratory tract contained an increased number of T lymphocytes, cells known to release monocyte chemotactic factor in sarcoidosis. Consistent with the knowledge that corticosteroids usually suppress the alveolitis of active sarcoidosis, when the expression of alveolar macrophage surface antigens was evaluated before and during therapy, the percentage of alveolar macrophages expressing monocyte-lineage surface antigens returned to normal after 1 to 3 mo of therapy.(ABSTRACT TRUNCATED AT 400 WORDS)