期刊
PLOS PATHOGENS
卷 9, 期 6, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.ppat.1003409
关键词
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资金
- Ministry of Education, Culture, Sports, Science and Technology (MEXT) [23000012, 23790472]
- Naito Foundation
- Grants-in-Aid for Scientific Research [25460527, 25670167, 23000012, 24390100, 23790472] Funding Source: KAKEN
NF-kappa B plays a central role in modulating innate immune responses to bacterial infections. Therefore, many bacterial pathogens deploy multiple mechanisms to counteract NF-kappa B activation. The invasion of and subsequent replication of Shigella within epithelial cells is recognized by various pathogen recognition receptors as pathogen-associated molecular patterns. These receptors trigger innate defense mechanisms via the activation of the NF-kappa B signaling pathway. Here, we show the inhibition of the NF-kappa B activation by the delivery of the IpaH E3 ubiquitin ligase family member IpaH0722 using Shigella's type III secretion system. IpaH0722 dampens the acute inflammatory response by preferentially inhibiting the PKC-mediated activation of NF-kappa B by ubiquitinating TRAF2, a molecule downstream of PKC, and by promoting its proteasome-dependent degradation.
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