UnZIPping Mechanisms of Effector-Triggered Immunity in Animals

Division of Infectious Diseases, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Cell host & microbe (Impact Factor: 12.33). 04/2012; 11(4):320-2. DOI: 10.1016/j.chom.2012.04.002
Source: PubMed


The mechanisms by which epithelial cells distinguish pathogens from commensal microbes have long puzzled us. Now, McEwan et al. (2012) and Dunbar et al. (2012), in this issue of Cell Host & Microbe, demonstrate that in C. elegans, microbial toxin-induced inhibition of host cellular functions, especially blockade of protein translation, activates the effector-triggered immune response dependent on the transcription factor ZIP-2.

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Available from: Anni Kleino
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    • "The third checkpoint may be the sensing of virulence factors or their activity, although it has to be said that commensals can also possess virulence factors such as type III secretion systems, and what may count more is whether micro-organisms have breached the mucosal layer (Swiatczak et al., 2011). Possibly hosts actually sense changes in their own metabolism as well, for example changes in transcription and translation (Kleino and Silverman, 2012). One key component appears to be the up-regulation of a transcription factor, ZIP-2, and transcription of its target genes, "
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