This study by Wang et al. identifies a role for the T-box transcription factor TBX1 in mediating tissue repair after myocardial infarction. TBX1 is of note clinically as its haploinsufficiency is linked to the cardiovascular and thymic developmental abnormalities seen in DiGeorge syndrome (also known as 22q11.2 deletion syndrome). Using mouse models of myocardial infarction, the authors found that Tbx1 is upregulated by lymphatic endothelial cells (LECs) during the reparative phase that occurs after myocardial infarction, and that Tbx1 expression promotes neo-lymphangiogenesis and repair responses in the heart. Key to this was TBX1-mediated induction of an immunosuppressive programme, which concentrated tolerogenic dendritic cells and regulatory T cells at ‘immune hubs’ with activated LECs. These immune hubs prevented the expansion of potentially autoreactive CD8+ T cells in the damaged heart and instead supported the expansion of reparative macrophage populations.