DC subsets of the murine healthy heart consisted of IRF8-dependent conventional (c)DC1,  IRF4-dependent cDC2 and monocyte-derived DCs. In steady state, cardiac self-antigen -myosin was presented in heart-draining mediastinal lymph node (mLN) by cDC1s, driving the proliferation of antigen-specific CD4+ TCR-M T cells, and their differentiation into Tregs. Following MI, all DC subsets infiltrated the heart, while only cDCs migrated to the mLN. Here, cDC2s induced TCR-M proliferation and differentiation into IL-17/IFN producing effector cells. Thus, cardiac specific autoreactive T cells get activated by mature DCs following myocardial infarction. SOURCE: Bart Lambrecht VIB-University of Ghent

Pluto Bioinformatics

GSE94949: Myocardial infarction (MI) primes autoreactive T cells through activation of dendritic cells