Young M R
Research Service, Department of Veterans Affairs, Hines VA Hospital, IL, USA.
Cancer Metastasis Rev. 1994 Dec;13(3-4):337-48. doi: 10.1007/BF00666103.
Studies in both cancer patients and in animal tumor models have shown that immune defenses can mediate destruction of tumor, but these defenses are often functioning at a suppressed or suboptimal level. Frequently, prostaglandins, mainly PGE2, have been implicated in this tumor-associated subversion of immune function, with immune reactivities to tumor typically being enhanced by prostaglandin synthesis inhibitor. Both the tumor and tumor-induced host immune suppressive macrophages have the capacity to suppress immune functions through their production of PGE2. Although the inhibitory functions have been more widely studied, recent evaluations of the effects of PGE2 have led to the surprising realization that not all of the PGE2's effects are inhibitory to immune function. Summarized below are some of the well characterized inhibitory effects of PGE2, as well as the lesser studied stimulatory effects of PGE2 toward the effector cells that are considered to be important in the immune defense against cancer.
对癌症患者和动物肿瘤模型的研究均表明,免疫防御能够介导肿瘤的破坏,但这些防御功能常常处于受抑制或次优水平。通常,前列腺素,主要是PGE2,被认为与这种肿瘤相关的免疫功能颠覆有关,前列腺素合成抑制剂通常会增强对肿瘤的免疫反应性。肿瘤以及肿瘤诱导的宿主免疫抑制巨噬细胞均有能力通过产生PGE2来抑制免疫功能。尽管对其抑制功能的研究更为广泛,但最近对PGE2作用的评估却意外地发现,并非PGE2的所有作用都是抑制免疫功能的。以下总结了PGE2一些已得到充分表征的抑制作用,以及对被认为在抗癌免疫防御中重要的效应细胞具有的、研究较少的刺激作用。