Tbx1 orchestrates an immune niche that safeguards a broken heart

Cardiac lymphatics cooperate with the reparative immune response in myocardial healing after infarction. In this issue of Immunity, Wang and colleagues discover a mechanism underlying this cooperation, dependent on the transcription factor Tbx1 and responsible for the creation of an immunosuppressive niche that mitigates autoimmunity. Cardiac lymphatics cooperate with the reparative immune response in myocardial healing after infarction. In this issue of Immunity, Wang and colleagues discover a mechanism underlying this cooperation, dependent on the transcription factor Tbx1 and responsible for the creation of an immunosuppressive niche that mitigates autoimmunity. Lymphatic endothelial transcription factor Tbx1 promotes an immunosuppressive microenvironment to facilitate post-myocardial infarction repairWang et al.ImmunityAugust 24, 2023In BriefMyocardial infarction (MI)-induced autoimmunity is detrimental, but it is usually resolved after the heart heals. However, the mechanism is unclear. Wang et al. report that Tbx1 upregulation in lymphatic endothelial cells enforces an immunosuppressive microenvironment to inhibit autoreactive CD8+ T cell expansion and increase reparative macrophages to repair post-MI damage. Full-Text PDF