Signaling and gene expression in inflammation

The Question

Not Too Little, Not Too Much, Just Right.

Effective defense against infectious agents and tissue-damaging cues requires rapid activation of inflammatory responses, followed by the timely re-establishment of immune homeostasis once the microbial threats have been eliminated. Insufficient responses lead to infectious disease, whereas failures in homeostatic control result in tissue damage and impaired healing. Therefore, inflammatory responses must be strong, but also precisely regulated in magnitude and duration. Our research aims to understand molecular mechanisms that drive the precise balance between pro- and anti-inflammatory processes and how these processes are coordinated such that healthy immunity is maintained.

The Approach

We investigate immune homeostasis and balanced immune responses in 3 areas:

1) mRNA decay. mRNA decay is fundamental for immune homeostasis and control of inflammation. We employ genome-wide approaches, systems biology and organismal models to reveal mechanisms defining the timely and selective removal of inflammation-associated mRNAs.

2) Transcription regulation by Mediator kinase. We investigate how Mediator kinase precisely adjusts transcriptional responses during inflammation using infection models, biochemistry, proteomics and genome-wide assays.

3) Cell signaling. We employ infection models to understand how cells and organisms integrate external and internal signaling events to launch efficient immune responses against pathogens.