Nuclear Factor κB (NF-κB) is a ubiquitously expressed transcription factor for genes involved in inflammation. The transcription of NF-κB-dependent genes can be altered by crosstalk with other signaling pathways. Recently, it has become evident that G-protein-coupled receptors (GPCRs) are implicated in immunity and that there is connectivity with NF-κB signaling. One of the GPCRs, that has received a lot of attention in the field of inflammatory research, is the β2-adrenergic receptor (β2-AR). Whereas it is generally accepted that β2-AR-mediated signals are anti-inflammatory, we observed thatin several cell types β2-AR agonists synergistically enhance the expression of particular NF-κB-dependent proinflammatory genes, while others are inhibited. In this project, we want to further explore the molecular basis of this selectivity. Special emphasis will be dedicated to nuclear crosstalk events, including actions of β2-AR agonists on chromatin remodeling and enhanceosome composition of NF-κB-dependent promoters.