Abstract
Cells engaging in inflammation undergo drastic changes of their transcriptomes. In order to tailor these alterations in gene expression to the requirements of the inflammatory process, tight and coordinate regulation of gene expression by environmental cues, microbial or danger-associated molecules or cytokines, are mandatory. The transcriptional response is set off by signal-regulated transcription factors (SRTFs) at the receiving end of pathways originating at pattern recognition- and cytokine receptors. These interact with a genome that has been set for an appropriate response by prior activity of pioneer or lineage determining transcription factors (LDTFs). The same types of transcription factors are also critical determinants of the changes in chromatin landscapes and transcriptomes that specify potential consequences of inflammation: tissue repair, training, and tolerance. Here we focus on the role of three families of SRTFs in inflammation and its sequels: signal transducers and activators of transcription (STATs), interferon regulatory factors (IRFs), and nuclear factor κB (NFκB). We describe recent findings about their interactions and about their networking with LDTFs. Our aim is to provide a snapshot of a highly dynamic research area.