MEMBRANE-FORM TUMOR NECROSIS FACTOR : ANALYSIS AND CLINICAL APPLECATION OF ACTIVATED ALVEOLAR MACROPHAGES

检测了人肺泡巨噬细胞(AM)和健康献血员外周血单核细胞膜形式肿瘤坏死因子(m-TNF)的表达。在脂多糖(LPS)刺激下，AM在其细胞表面产生26-kDa的肿瘤坏死因子-α。我们设计了一种测定m-肿瘤坏死因子的生物测定方法，将巨噬细胞刺激18小时后用多聚甲醛固定，然后检测固定的巨噬细胞对L929细胞的细胞毒作用。在内毒素刺激下，AM产生m-TNF的时间明显早于分泌TNF-α的时间。IL-4对m-TNF的产生和分泌均有抑制作用。虽然单核细胞产生少量的m-肿瘤坏死因子，但单核细胞来源的巨噬细胞在GM-CSF培养10天后表现出增强的m-肿瘤坏死因子。作为一种生物活性，活化的单核细胞上的m-肿瘤坏死因子显著增加了肺癌细胞系RERF-LC-OK细胞产生IL-6。提示m-肿瘤坏死因子可能在原位展示噬菌体功能中发挥重要作用。

The expressions of a membrane form TNF (m-TNF) by human alveolar macrophages (AM) and autologous blood monocytes from healthy donors were examined. Upon lipopolysaccharide (LPS) stimulation, AM produced 26-kDa TNF-alpha on thier cell surface. We designed a bioassay for measuring m-TNF in which macrophages were fixed with paraformaldehyde after stimulation for 18hr, then m-TNF activity was assessed as cytotoxicity of fixed macrophages on L929 cells. on LPS istmulation, AM produced significant amounts of m-TNF earlier than TNF-alpha secretion. Interleukin-4 suppressed both m-TNF producition and TNF-alpha secretion. Although blood monocytes produced small amounts of m-TNF, monocyte-derived macrophages showed enhanced m-TNF after cultivation with GM-CSF for 10 days. as a biological activity, m-TNF on activated monocytes significantly augmented interleukin-6 production by a lung cancer cell line, RERF-LC-OK cells. These findings suggest that m-TNF may play important roles in exhibition of amcrophage functions in situ.