期刊
PLOS PATHOGENS
卷 12, 期 5, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.ppat.1005653
关键词
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资金
- Medical Research Council [MR/K027077/1]
- Wellcome Trust [095484/Z/11/Z]
- European Molecular Biology Organization [ATFL1177-2007]
- Medical Research Council [MR/J006874/1, MR/K027077/1] Funding Source: researchfish
- Wellcome Trust [095484/Z/11/Z] Funding Source: Wellcome Trust
- MRC [MR/K027077/1, MR/J006874/1] Funding Source: UKRI
Salmonella enterica replicates in macrophages through the action of effector proteins translocated across the vacuolar membrane by a type III secretion system (T3SS). Here we show that the SPI-2 T3SS effector SpvD suppresses proinflammatory immune responses. SpvD prevented activation of an NF-kappa B-dependent promoter and caused nuclear accumulation of importin-a, which is required for nuclear import of p65. SpvD interacted specifically with the exportin Xpo2, which mediates nuclear-cytoplasmic recycling of importins. We propose that interaction between SpvD and Xpo2 disrupts the normal recycling of importin-a from the nucleus, leading to a defect in nuclear translocation of p65 and inhibition of activation of NF-kappa B regulated promoters. SpvD down-regulated pro-inflammatory responses and contributed to systemic growth of bacteria in mice. This work shows that a bacterial pathogen can manipulate host cell immune responses by interfering with the nuclear transport machinery.
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