Journal
IMMUNITY
Volume 23, Issue 3, Pages 319-329Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2005.08.010
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Funding
- NIAID NIH HHS [R01 AI 061712] Funding Source: Medline
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Certain microbes evade host innate immunity by killing activated macrophages with the help of virulence factors that target prosurvival pathways. For instance, infection of macrophages with the TLR4-activating bacterium Bacillus anthracis triggers an apoptotic response due to inhibition of p38 MAP kinase activation by the bacterial-produced lethal toxin. Other pathogens induce macrophage apoptosis by preventing activation of NF-kappa B, which depends on I kappa B kinase beta (IKK beta). To better understand how p38 and NF-kappa B maintain macrophage survival, we searched for target genes whose products prevent TLR4-induced apoptosis and a p38-dependent transcription factor required for their induction. Here we describe key roles for transcription factor CREB, a target for p38 signaling, and the plasminogen activator 2 (PAI-2) gene, a target for CREB, in maintenance of macrophage survival.
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