Institute of Biochemistry I/ZAFES, Faculty of Medicine, Goethe-University Frankfurt, 60590 Frankfurt, Germany.
Immunobiology. 2012 Dec;217(12):1225-32. doi: 10.1016/j.imbio.2012.05.001. Epub 2012 May 11.
Extensive research in the last two decades implemented that the inflammatory cell infiltrate, especially in solid tumors, is a major determinant for patient prognosis. Mononuclear phagocytes, i.e. monocytes/macrophages, dendritic cells and myeloid-derived suppressor cells, constitute the majority of tumor-associated immune cells. Instead of inducing anti-tumor immunity, mononuclear phagocytes are functionally subverted by tumor microenvironmental factors to support each stage of oncogenesis. Although mechanisms how tumors program their inflammatory infiltrate to support tumor development are ill-defined, few master regulators are beginning to emerge. One of them is the inflammatory eicosanoid prostaglandin E(2) (PGE(2)), produced by tumor cells or the infiltrating immune cells. In this review we summarize the impact of PGE(2) on mononuclear phagocytes in inflammation and cancer and discuss potential implications for cancer therapy.
在过去的二十年中，大量研究表明，炎症细胞浸润，特别是在实体肿瘤中，是患者预后的主要决定因素。单核吞噬细胞，即单核细胞/巨噬细胞、树突状细胞和髓系来源的抑制细胞，构成了大多数与肿瘤相关的免疫细胞。单核吞噬细胞没有诱导抗肿瘤免疫，而是被肿瘤微环境因素在功能上颠覆，以支持肿瘤发生的各个阶段。尽管肿瘤如何编程其炎症浸润以支持肿瘤发展的机制尚不清楚，但一些主要的调控因子开始显现。其中之一是炎症类二十烷素前列腺素 E2（PGE2），由肿瘤细胞或浸润的免疫细胞产生。在这篇综述中，我们总结了 PGE2 对炎症和癌症中单核吞噬细胞的影响，并讨论了其对癌症治疗的潜在意义。
