Burleigh Barbara A, Woolsey Aaron M
Department of Immunology and Infectious Diseases, Harvard School of Public Health, 665 Huntington Ave, Bldg I Rm 713, Boston, MA 02115, USA.
Cell Microbiol. 2002 Nov;4(11):701-11. doi: 10.1046/j.1462-5822.2002.00226.x.
Mammalian cell invasion by the protozoan pathogen Trypanosoma cruzi is critical to its survival in the host. To promote its entry into a wide variety of non-professional phagocytic cells, infective trypomastigotes exploit an arsenal of heterogenous surface glycoproteins, secreted proteases and signalling agonists to actively manipulate multiple host cell signalling pathways. Signals initiated in the parasite upon contact with mammalian cells also function as critical regulators of the invasion process. Whereas the full spectrum of cellular responses modulated by T. cruzi is not yet known, mounting evidence suggests that these pathways impinge on a number of cellular processes, in particular the ubiquitous wound-repair mechanism exploited for lysosome-mediated parasite entry. Furthermore, differential engagement of host cell signalling pathways in a cell type-specific manner and modulation of host cell gene expression by T. cruzi are becoming recognized as essential determinants of infectivity and intracellular survival by this pathogen.
原生动物病原体克氏锥虫对哺乳动物细胞的侵袭对其在宿主体内的存活至关重要。为促进其进入多种非专职吞噬细胞，感染性锥鞭毛体利用一系列异源表面糖蛋白、分泌型蛋白酶和信号激动剂来积极操控多个宿主细胞信号通路。寄生虫与哺乳动物细胞接触后启动的信号也作为侵袭过程的关键调节因子发挥作用。虽然克氏锥虫调节的细胞反应全貌尚不清楚，但越来越多的证据表明，这些信号通路影响许多细胞过程，特别是用于溶酶体介导的寄生虫进入的普遍存在的伤口修复机制。此外，宿主细胞信号通路以细胞类型特异性方式的差异参与以及克氏锥虫对宿主细胞基因表达的调节正被认为是该病原体感染性和细胞内存活的重要决定因素。
