Extended Data Fig. 10: Summary.

Mutations in the epigenetic regulators Dnmt3a or Tet2 in hematopoietic cells converge in the emergence of a distinct macrophage subset in the arterial adventitia (denoted CHIP Resident-like Mφ) that combines surface markers associated with resident-like macrophages (depicted: mannose receptor/CD206) with a distinct inflammatory chemokine signature. These cells are surrounded by other myeloid cells and clusters of activated endothelium. Overall, lesional (inflammatory) macrophage content increases, while other immune cell subsets, in particular T lymphocytes, decrease. Collectively, these processes result in increased atherosclerosis.