Neuroendocrine system modulation of T cell responses after myocardial infarction (B1)

Rationale and aims

We hypothesize that neuroendocrine system regulates T cell responses towards a pro-healing phenotype. We will test this hypothesis by studying the effects of β-adrenergic and natriuretic peptide signalling on T cell functions and their contribution to cardiac inflammation and healing after infarction.

Approach

We will use genetic models aligned to cell transfer experiments to address the role of β2-adrenergic, GC-A natriuretic peptide receptors and Pde2a, an enzyme that controls both pathways, in T cell responses after myocardial infarction. Those responses will be characterized by complementarily high-end multi-colour light-sheet fluorescence microscopy, flow cytometry , cAMP/cGMP FRET analysis and single-cell sequencing. In addition, cardiac function will be monitored by 4-chamber echocardiography and magnetic resonance imaging.