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Immunol Res. 2013 Dec;57(1-3):237-45. doi: 10.1007/s12026-013-8454-3.

The Yersinia pestis type III secretion system: expression, assembly and role in the evasion of host defenses.

Author information

1
Department of Microbiology and Immunology, University of Miami Miller School of Medicine, 1600 NW 10th Avenue, Miami, FL, 33136, USA, gplano@med.miami.edu.

Abstract

Yersinia pestis, the etiologic agent of plague, utilizes a type III secretion system (T3SS) to subvert the defenses of its mammalian hosts. T3SSs are complex nanomachines that allow bacterial pathogens to directly inject effector proteins into eukaryotic cells. The Y. pestis T3SS is not expressed during transit through the flea vector, but T3SS gene expression is rapidly thermoinduced upon entry into a mammalian host. Assembly of the T3S apparatus is a highly coordinated process that requires the homo- and hetero-oligomerization over 20 Yersinia secretion (Ysc) proteins, several assembly intermediates and the T3S process to complete the assembly of the rod and external needle structures. The activation of effector secretion is controlled by the YopN/TyeA/SycN/YscB complex, YscF and LcrG in response to extracellular calcium and/or contact with a eukaryotic cell. Cell contact triggers the T3S process including the secretion and assembly of a pore-forming translocon complex that facilitates the translocation of effector proteins, termed Yersinia outer proteins (Yops), across the eukaryotic membrane. Within the host cell, the Yop effector proteins function to inhibit bacterial phagocytosis and to suppress the production of pro-inflammatory cytokines.

PMID:
24198067
DOI:
10.1007/s12026-013-8454-3
[Indexed for MEDLINE]

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