Abstract：
Studies spanning the last 3 decades have fundamentally altered our understanding of the interplay between the hemostatic and immune systems. A plethora of studies have revealed that there is bidirectional crosstalk between these two systems at multiple levels that likely evolved as a means to coordinate the host response to numerous challenges, including trauma, infection, and thermal or chemical injury. Such challenges require reestablishment of vascular integrity, the clearance of pathogens, and removal of cellular and external debris. Clearly, bidirectional coordination of hemostasis and immunity would be beneficial in such contexts. Many types of malignancies take advantage of the interplay between hemostasis and immunity, co-opting these mechanisms to promote tumorigenesis, the formation of a supportive stroma, and metastasis to distant organs. Three important \"bridges\" that mechanistically link the hemostatic system to immune functions that have been shown to play a key role in cancer biology include the platelet/fibrinogen axis, protease activated receptor-1 (PAR-1) and protease activated receptor-2 (PAR-2). These hemostatic system components have been shown to regulate a variety of immune functions that support tumorigenesis in the context of inflammation-driven malignancy, metastasis, and escape from adaptive antitumor immunity. Understanding the mechanisms coupling these bridges between hemostasis and immunity, as well as others, could provide novel targets for the prevention and treatment of a variety of cancers.
摘要：
过去30年的研究从根本上改变了我们对止血系统和免疫系统之间相互作用的理解。大量研究表明，这两个系统之间存在多层次的双向串扰，这可能是协调主机应对众多挑战的一种手段。包括外伤,感染,热或化学损伤。这些挑战需要重建血管的完整性，病原体的清除，去除细胞和外部碎片。显然,在这种情况下，止血和免疫的双向协调将是有益的。许多类型的恶性肿瘤利用止血和免疫之间的相互作用，选择这些机制来促进肿瘤发生，支持性基质的形成，转移到远处器官。三个重要的“桥梁”，已被证明在癌症生物学中发挥关键作用的免疫功能的机制连接止血系统，包括血小板/纤维蛋白原轴，蛋白酶激活受体-1(PAR-1)和蛋白酶激活受体-2(PAR-2)。这些止血系统成分已被证明可以调节多种免疫功能，在炎症驱动的恶性肿瘤的背景下支持肿瘤发生。转移,逃避适应性抗肿瘤免疫。了解止血和免疫之间这些桥梁的耦合机制，以及其他人,可以为多种癌症的预防和治疗提供新的靶点。
