Evasion of innate immunity by parasitic protozoa

被引：278

作者：

Sacks, D ^{[1
]}

Sher, A ^{[1
]}

机构：

[1] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA

来源：

NATURE IMMUNOLOGY | 2002年 / 3卷 / 11期

关键词：

D O I：

10.1038/ni1102-1041

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Parasitic protozoa are a major cause of global infectious disease. These eukaryotic pathogens have evolved with the vertebrate immune system and typically produce long-lasting chronic infections. A critical step in their host interaction is the evasion of innate immune defenses. The ability to avoid attack by humoral effector mechanisms, such as complement lysis, is of particular importance to extracellular parasites, whereas intracellular protozoa must resist killing by lysosomal enzymes and toxic metabolites. They do so by remodeling the phagosomal compartments in which they reside and by interfering with signaling pathways that lead to cellular activation. In addition, there is growing evidence that protozoan pathogens modify the antigen-presenting and immunoregulatory functions of dendritic cells, a process that facilitates their evasion of both innate and adaptive immunity.

引用

页码：1041 / 1047

页数：7

共 99 条

[91] Human dendritic cells discriminate between viable and killed Toxoplasma gondii tachyzoites:: Dendritic cell activation after infection with viable parasites results in CD28 and CD40 ligand signaling that controls IL-12-dependent and -independent T cell production of IFN-γ [J].