Yamin M, Lazarus D, Schneeberger E E, McCarthy K, Xia W J, Kradin R
Department of Pathology, Massachusetts General Hospital, Boston 02114.
Am J Respir Cell Mol Biol. 1990 Feb;2(2):207-15. doi: 10.1165/ajrcmb/2.2.207.
Activated macrophages participate in inflammation by eliminating foreign cells, promoting wound healing, and modulating the immune response. A murine monoclonal antibody, designated anti-rat macrophage activator (RMA), was raised against alveolar macrophages (AM) activated with interferon-gamma (IFN-gamma) and phorbol myristate acetate (PMA). The RMA antigen is expressed by resident macrophages but not by other cells. Binding to AM by anti-RMA is not competitively inhibited by the murine monoclonal antibodies MRC OX-41, OX-42, and OX-43. Surface membrane expression of RMA antigens is upregulated by lipopolysaccharide, PMA, and tumor necrosis factor-alpha but not by IFN-gamma. Stimulation of AM with anti-RMA yields distinct ultrastructural alterations, as well as de novo protein and DNA synthesis. Immunoprecipitation of [35S]methionine metabolically labeled AM yields a 120 kD protein by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) that is not altered by chemical reduction. We conclude that the RMA antigen is macrophage specific and that binding of anti-RMA to AM promotes functional activities in a subset of these cells.
活化的巨噬细胞通过清除外来细胞、促进伤口愈合和调节免疫反应参与炎症过程。一种鼠单克隆抗体，命名为抗大鼠巨噬细胞激活剂（RMA），是针对用γ干扰素（IFN-γ）和佛波醇肉豆蔻酸酯乙酸酯（PMA）激活的肺泡巨噬细胞（AM）产生的。RMA抗原由驻留巨噬细胞表达，而其他细胞不表达。抗RMA与AM的结合不受鼠单克隆抗体MRC OX-41、OX-42和OX-43的竞争性抑制。RMA抗原的表面膜表达可被脂多糖、PMA和肿瘤坏死因子-α上调，但不被IFN-γ上调。用抗RMA刺激AM会产生明显的超微结构改变，以及新的蛋白质和DNA合成。通过十二烷基硫酸钠-聚丙烯酰胺凝胶电泳（SDS-PAGE）对[35S]甲硫氨酸代谢标记的AM进行免疫沉淀，得到一种120 kD的蛋白质，其不受化学还原的影响。我们得出结论，RMA抗原是巨噬细胞特异性的，抗RMA与AM的结合促进了这些细胞亚群中的功能活动。
