DosReis G A, Barcinski M A
Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Brazil.
Adv Parasitol. 2001;49:133-61. doi: 10.1016/s0065-308x(01)49039-7.
Apoptosis, a form of programmed cell death (PCD), plays a central role in normal tissue development as well as in the pathogenesis of different diseases. PCD is responsible for the non-inflammatory physiological elimination of potentially harmful or unnecessary cells during embryogenesis, and for the proper functioning of continuous cell renewal systems in adult organisms. Maturation of the immune system and the specific immune response are examples of situations where PCD plays important roles. This review discusses the importance of apoptosis in two fundamental elements of a host-parasite interaction: the parasite (Section 1), and the host's immune response (Section 2). Section 1 discusses questions raised by the description of apoptosis in unicellular eukaryotes, such as the evolutionary origin of the molecular components of PCD, its role in the emergence and maintenance of parasitism, and the constraints of a multicellular organization for the proper operation of a cell death programme. The proposal is that PCD can occur in any situation where living cells display features of an organized network which operates through interactions within themselves and/or with elements of their environment. The possibility is also discussed that evolutionary relics of a complete cell death system may operate in unicellular parasites with functions other than inducing cell death. Section 2 reviews data on the mechanisms of host-cell PCD and the consequences of this phenomenon in host defence and pathogenesis. Infectious agents, from viruses to parasites, can either delay or induce apoptosis of different types of host cells. Apoptosis following lymphocyte polyclonal activation and stimulation of peripheral T lymphocytes, as a result of the engagement of specific counter-receptor systems, is of special interest for defining host immunocompetence and mechanisms of immunopathology.
细胞凋亡是程序性细胞死亡(PCD)的一种形式,在正常组织发育以及不同疾病的发病机制中都起着核心作用。PCD负责在胚胎发育过程中对潜在有害或不必要的细胞进行非炎性生理性清除,以及在成年生物体中维持连续细胞更新系统的正常功能。免疫系统的成熟和特异性免疫反应就是PCD发挥重要作用的例子。本综述讨论了细胞凋亡在宿主-寄生虫相互作用的两个基本要素中的重要性:寄生虫(第1节)和宿主的免疫反应(第2节)。第1节讨论了单细胞真核生物中细胞凋亡描述所引发的问题,例如PCD分子成分的进化起源、其在寄生现象出现和维持中的作用,以及多细胞组织对细胞死亡程序正常运作的限制。有人提出,只要活细胞表现出通过自身内部相互作用和/或与环境要素相互作用而运作的有组织网络的特征,PCD就可能发生。还讨论了完整细胞死亡系统的进化遗迹可能在单细胞寄生虫中发挥作用,但其功能并非诱导细胞死亡的可能性。第2节综述了关于宿主细胞PCD机制的数据以及这一现象在宿主防御和发病机制中的后果。从病毒到寄生虫的感染因子,既可以延迟也可以诱导不同类型宿主细胞的凋亡。淋巴细胞多克隆激活和外周T淋巴细胞刺激后由于特异性反受体系统的参与而导致的细胞凋亡,对于确定宿主免疫能力和免疫病理机制特别有意义。