Matsuno Stephanie Y, Pandori William J, Lodoen Melissa B
Department of Molecular Biology & Biochemistry, University of California, Irvine, Irvine, CA 92617 USA.
Department of Molecular Biology & Biochemistry, University of California, Irvine, Irvine, CA 92617 USA.
Curr Opin Microbiol. 2023 Apr;72:102264. doi: 10.1016/j.mib.2023.102264. Epub 2023 Feb 13.
Intracellular pathogens strike a delicate balance between maintaining their survival within infected cells, while also activating host defense mechanisms. Toxoplasma gondii is a protozoan parasite that initiates a variety of host signaling pathways as it invades host cells and establishes residence in a parasitophorous vacuole. Recent work has highlighted the interplay between T. gondii infection and innate immune pathways that lead to inflammation, several of which converge on caspases. This family of cysteine proteases function at the crossroads of inflammation and cell death and serve as a key target for parasite manipulation. This review focuses on the interaction of T. gondii with caspase-dependent inflammatory and cell death pathways and the role of parasite effector proteins in modulating these processes.
细胞内病原体在维持其在受感染细胞内的生存与激活宿主防御机制之间达成了微妙的平衡。刚地弓形虫是一种原生动物寄生虫，在侵入宿主细胞并在寄生泡中定居时会启动多种宿主信号通路。最近的研究突出了刚地弓形虫感染与导致炎症的先天免疫途径之间的相互作用，其中有几种途径汇聚于半胱天冬酶。这个半胱氨酸蛋白酶家族在炎症和细胞死亡的交叉点发挥作用，并且是寄生虫操控的关键靶点。本综述聚焦于刚地弓形虫与半胱天冬酶依赖性炎症和细胞死亡途径的相互作用，以及寄生虫效应蛋白在调节这些过程中的作用。
