Inflammation involves the activation of a highly coordinated gene expression 
program that is specific for the initial stimulus and occurs in a different 
manner in bystander parenchymal cells and professional immune system cells 
recruited to the inflamed site. Recent data demonstrate that developmental 
transcription factors like the macrophage fate-determining Pu.1 set the stage 
for the activity of ubiquitous transcription factors activated by inflammatory 
stimuli, like NF-kB, AP-1, and interferon regulatory factors (IRFs). The 
intersection of lineage-determining and stimulus-activated transcription factors 
at enhancers explains cell type specificity in inflammatory responses.