Sica Antonio, Porta Chiara, Morlacchi Sara, Banfi Stefania, Strauss Laura, Rimoldi Monica, Totaro Maria Grazia, Riboldi Elena
DiSCAFF, University of Piemonte Orientale A. Avogadro, via Bovio 6, 28100, Novara, Italy,
Cancer Microenviron. 2012 Aug;5(2):133-49. doi: 10.1007/s12307-011-0091-6. Epub 2011 Sep 24.
The construction of an inflammatory microenvironment provides the fuel for cancer development and progression. Hence, solid tumors promote the expansion and the recruitment of leukocyte populations, among which tumor-associated myeloid cells (TAMCs) represent a paradigm for cancer-promoting inflammation. TAMCs group heterogeneous phagocytic populations stemming from a common myeloid progenitor (CMP), that orchestrate various aspects of cancer, including: diversion and skewing of adaptive responses; immunosuppression; cell growth; angiogenesis; matrix deposition and remodelling; construction of a metastatic niche and actual metastasis. Several evidence indicate that TAMCs show plasticity and/or functional heterogeneity, suggesting that tumour-derived factors promote their functional "reprogramming" towards protumoral activities. While recent studies have attempted to address the role of microenvironment signals, the interplay between cancer cells, innate and adaptive immunity is now emerging as a crucial step of the TAMCs reprogramming. Here we discuss the evidence for the differentiation of TAMCs during the course of tumor progression and the molecular mechanisms that regulate such event.
炎性微环境的构建为癌症的发生和发展提供了助力。因此,实体瘤会促进白细胞群体的扩增和募集,其中肿瘤相关髓样细胞(TAMCs)是促癌炎症的一个典型例子。TAMCs 包含源自共同髓样祖细胞(CMP)的异质性吞噬细胞群体,它们在癌症的各个方面发挥作用,包括:适应性反应的转向和偏差;免疫抑制;细胞生长;血管生成;基质沉积和重塑;转移微环境的构建以及实际转移。多项证据表明,TAMCs 具有可塑性和/或功能异质性,这表明肿瘤衍生因子促使它们向促肿瘤活性进行功能性“重编程”。虽然最近的研究试图探讨微环境信号的作用,但癌细胞、固有免疫和适应性免疫之间的相互作用正逐渐成为 TAMCs 重编程的关键步骤。在此,我们讨论肿瘤进展过程中 TAMCs 分化的证据以及调节这一过程的分子机制。