Keller R, Keist R, Frei K
Immunbiology Research Group, University of Zurich, Switzerland.
Eur J Immunol. 1990 Mar;20(3):695-8. doi: 10.1002/eji.1830200334.
The abilities of various macrophage-activating agents to trigger tumoricidal activity and/or the secretion of prostaglandin E2 (PGE2), interleukin 6 (IL 6) and transforming growth factor beta (TGF beta) in bone marrow-derived mononuclear phagocytes (BMM phi) in vitro were comparatively assessed. Induction of tumoricidal activity by lymphokines, that is only short-lived, was not associated with enhanced secretion of these activities by BMM phi; in contrast, incubation with heat-killed facultative intracellular bacteria resulted in persisting tumoricidal activity and in marked enhancement of the secretion of IL 6 and PGE2, but not of TGF beta activity. These findings support the concept that the pattern of the secretory response induced in macrophages by lymphokines differs from that triggered by bacteria and that the rapid decay of lymphokine-induced tumoricidal activity is not due to autocrine macrophage deactivation mediated by one of these agents alone.
对多种巨噬细胞激活剂在体外触发骨髓来源的单核吞噬细胞（BMM phi）的杀肿瘤活性和/或前列腺素E2（PGE2）、白细胞介素6（IL 6）及转化生长因子β（TGF beta）分泌的能力进行了比较评估。淋巴因子诱导的杀肿瘤活性只是短暂存在，且与BMM phi增强分泌这些活性物质无关；相反，与热灭活的兼性细胞内细菌孵育会导致持续的杀肿瘤活性以及IL 6和PGE2分泌显著增强，但TGF beta活性无增强。这些发现支持这样的概念，即淋巴因子在巨噬细胞中诱导的分泌反应模式不同于细菌触发的模式，且淋巴因子诱导的杀肿瘤活性的快速衰减并非仅由这些因子之一介导的自分泌巨噬细胞失活所致。
