Monocytes dominate the cellular infiltrate in the first days after myocardial infarction, and participate to infarct wound healing. Importantly, monocyte differentiation and functional adaptation from specialization for cell debris removal towards supporting myocardial healing is driven by the local cytokine milieu. Whether regulatory T cells dictate monocyte differentiation and therefore the cardiac function after infarction is still unclear.
Rationale and aims
In this project we will elucidate how monocytes and Treg cell subsets regulate these processes and specifically focus on how myeloid and lymphoid populations communicate and interact in order to execute their concerted function.
We will complementarily use novel mouse models, high-end multi-colour fluorescence approaches such as light-sheet fluorescence microscopy and multicolour flow cytometry, and single-cell sequencing, to track and phenotype monocytes and their progeny as well as regulatory T cells, and investigate how these are influenced by type IL1-family and prototypical anti-inflammatory cytokines after myocardial infarction.
Significance and outlook
By investigating the molecular mechanisms and fundamental aspects of these two important cellular elements we expect to identify new molecular mechanisms that will allow for directed, therapeutic interventions in the future.
Medizinische Klinik und Poliklinik I, Universitätsklinikum Würzburg, Zentrum für Innere Medizin (ZIM), Oberdürrbacher Straße 6, Haus A3, 97080 Würzburg, Deutschland
Deutsches Zentrum für Herzinsuffizienz Würzburg | Comprehensive Heart Failure Center | Am Schwarzenberg 15 | Haus A15 | 97078 Würzburg