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Immunol Res. 2004;29(1-3):175-86.

Bacterial inhibition of eukaryotic pro-inflammatory pathways.

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Department of Pathology, Emory University School of Medicine, 105-F Whitehead Memorial Research Building, 615 Michaels Street, Atlanta, GA 30322, USA.


Eukaryotic cells perceive and respond to microbes, both pathogenic and commensal, by activation of signaling cascades such as the NF-kappaB pathway. Induction of such pathways leads to the upregulation of a program of gene expression that mediates pro-inflammatory and anti-apoptotic effector proteins. This host response is usually effective in clearing or controlling an infection. For pathogens (and potentially, symbionts) to continue their lifecycle, it is necessary to evade or repress these cellular responses. There has been recent interest in bacteria that can inhibit pro-inflammatory pathways, in some cases by the actions of soluble effector proteins secreted via a Type III secretion system. Certain effector proteins with this function possess enzymatic activity toward ubiquitin and related molecules. Ubiquitination is an increasingly recognized regulatory modification in eukaryotic cells, and microbial effectors that modulate this key host system may have diverse effects on infected cells and mediate many aspects of eukaryotic-prokaryotic interactions.

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