Hammerstrøm J
Acta Pathol Microbiol Scand C. 1980 Aug;88(4):201-9. doi: 10.1111/j.1699-0463.1980.tb00095.x.
Human effusion macrophages isolated from the pleural or ascitic effusions of 14 patients with malignant or benign disease usually inhibited methyl-3H-thymidine incorporation in an adherent human tumour cell line (NHIK 3025) when the macrophages were challenged with target cells immediately after isolation. The cytostatic activity disappeared when the macrophages were cultured for 18 hours in vitro before target cell challenge. The presence of endotoxin (LPS) or Corynebacterium parvum (Cp) during the macrophage-target cell interaction induced a small enhancement of the macrophage-mediated cytostatic activity. Preincubation of macrophages with Cp or Cp-induced lymphokine supernatants for 2-18 hours before target cell challenge induced increased cytostatic activity in the macrophage cultures. Adherent (NHIK 3025) or non-adherent (K-562) human tumour cells prelabelled with methyl-3H-thymidine, when added to freshly isolated macrophages, were lysed in a slowly progressive manner. The cytolytic activity to K-562 cells was enhanced by increasing macrophage density in the cultures, and by incubating the macrophages for 2 hours with lymphokine supernatants before target cell challenge. Morphological observations indicated that K-562 cells adhered to macrophage membranes, with lysis proceeding extracellularily.
从14例患有恶性或良性疾病患者的胸腔积液或腹水分离出的人渗出巨噬细胞,在分离后立即用靶细胞攻击时,通常会抑制贴壁人肿瘤细胞系(NHIK 3025)中甲基-3H-胸腺嘧啶核苷的掺入。当巨噬细胞在体外培养18小时后再进行靶细胞攻击时,其细胞抑制活性消失。在巨噬细胞与靶细胞相互作用期间存在内毒素(LPS)或短小棒状杆菌(Cp)会使巨噬细胞介导的细胞抑制活性略有增强。在靶细胞攻击前将巨噬细胞与Cp或Cp诱导的淋巴因子上清液预孵育2至18小时,可使巨噬细胞培养物中的细胞抑制活性增加。预先用甲基-3H-胸腺嘧啶核苷标记的贴壁(NHIK 3025)或非贴壁(K-562)人肿瘤细胞,当加入新鲜分离的巨噬细胞时,会以缓慢渐进的方式被裂解。通过增加培养物中巨噬细胞的密度,以及在靶细胞攻击前将巨噬细胞与淋巴因子上清液孵育2小时,可增强对K-562细胞的细胞溶解活性。形态学观察表明,K-562细胞粘附于巨噬细胞膜,裂解在细胞外进行。