Abstract
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-κB, which depends on IκB kinase β (IKKβ). To better understand how p38 and NF-κB 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.
Original language | English |
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Pages (from-to) | 319-329 |
Number of pages | 11 |
Journal | Immunity |
Volume | 23 |
Issue number | 3 |
DOIs | |
Publication status | Published - Sept 2005 |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Infectious Diseases