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Understanding how extracellular signals are linked to gene expression is a fundamental challenge in biology, and more specifically, macrophage signal integration is central to understanding healthy versus aberrant regulation of inflammation. My laboratory uses quantitative approaches to address these problems, with major projects including (1) computational modeling of signaling-to-transcription in macrophages, (2) interrogating tissue-specific macrophage signaling, and (3) dissecting molecular determinants of macrophage inflammatory function. We use both data-driven and mechanistic modeling approaches to integrate transcription factor activity, global phosphorylation, and transcriptomic data to explore signaling mechanisms that shape macrophage function. In the tissue context, we use a combination of network-based approaches and hypothesis driven in vivo experiments to identify mechanisms linking tissue stimuli (e.g. cytokines and lipids) to transcription factor activity, and ultimately macrophage function. We hope these efforts will yield insights into dysregulation of signaling and inflammation, while informing therapeutic strategies.