For a long time, host cell death during parasitic infection has been considered a reflection of tissue damage, and often associated with disease pathogenesis. However, during their evolution, protozoan and helminth parasites have developed strategies to interfere with cell death so as to spread and survive in the infected host, thereby ascribing a more intriguing role to infection-associated cell death. In this review, we examine the mechanisms used by intracellular and extracellular parasites to respectively inhibit or trigger programmed cell death. We further dissect the role of the prototypical “eat-me signal” phosphatidylserine (PtdSer) which, by being exposed on the cell surface of damaged host cells as well as on some viable parasites via a process of apoptotic mimicry, leads to their recognition and up-take by the neighboring phagocytes. Although barely dissected so far, the engagement of different PtdSer receptors on macrophages, by shaping the host immune response, affects the overall infection outcome in models of both protozoan and helminth infections. In this scenario, further understanding of the molecular and cellular regulation of the PtdSer exposing cell-macrophage interaction might allow the identification of new therapeutic targets for the management of parasitic infection.

长期以来，寄生虫感染期间的宿主细胞死亡被认为是组织损伤的反映，并且通常与疾病发病机制有关。然而，在它们的进化过程中，原生动物和蠕虫寄生虫已经开发出干扰细胞死亡的策略，以便在受感染的宿主中传播和生存，从而将更有趣的作用归因于与感染相关的细胞死亡。在这篇综述中，我们研究了细胞内和细胞外寄生虫分别抑制或触发程序性细胞死亡的机制。我们进一步剖析了原型“吃我信号”磷脂酰丝氨酸 (PtdSer) 的作用，它通过凋亡模拟过程暴露在受损宿主细胞的细胞表面以及一些存活的寄生虫上，导致它们的识别和被邻近的吞噬细胞摄取。尽管到目前为止几乎没有解剖过，但巨噬细胞上不同 PtdSer 受体的参与，通过塑造宿主免疫反应，影响原生动物和蠕虫感染模型中的整体感染结果。在这种情况下，进一步了解暴露细胞 - 巨噬细胞相互作用的 PtdSer 的分子和细胞调节可能有助于确定用于管理寄生虫感染的新治疗靶点。