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Regulatory Networks Involving STATs, IRFs, and NFκB in Inflammation
Ekaterini Platanitis1, Thomas Decker1
1Max F. Perutz Laboratories, Department of Microbiology, Immunobiology and Genetics, University of Vienna, Vienna, Austria.
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.
Insights
Inflammation drastically alters cell transcriptomes, requiring coordinated gene regulation by transcription factors. This study examines signal-regulated transcription factors (SRTFs) like STATs, IRFs, and NFκB in inflammation and its outcomes.
Area of Science:
- Molecular Biology
- Immunology
- Genetics
Background:
- Cellular inflammation involves significant transcriptome alterations.
- Gene expression must be tightly regulated by environmental cues and cytokines during inflammation.
- Signal-regulated transcription factors (SRTFs) initiate transcriptional responses to inflammatory signals.
Purpose of the Study:
- To investigate the role of three key SRTF families in inflammation and its consequences.
- To explore the interactions and networking of SRTFs with lineage determining transcription factors (LDTFs).
- To provide an updated overview of a rapidly evolving research field.
Main Methods:
- Focus on signal transducers and activators of transcription (STATs).
- Focus on interferon regulatory factors (IRFs).
- Focus on nuclear factor κB (NFκB).
Main Results:
- SRTFs interact with genomes pre-set by LDTFs for appropriate inflammatory responses.
- SRTFs are crucial for chromatin landscape and transcriptome changes.
- These changes dictate inflammation outcomes such as tissue repair, training, and tolerance.
Conclusions:
- STATs, IRFs, and NFκB are central players in inflammation and its sequels.
- Understanding SRTF and LDTF interactions is key to deciphering inflammatory processes.
- This research highlights the dynamic nature of transcription factor networks in immunity.
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