Fidler et al. show that anti-IL-1β treatment of atherosclerotic Ldlr-null mice with clonal expansion of Tet2-null or Jak2VF hematopoietic stem cells promotes the recruitment of fibroblast-like cells to the plaque fibrous cap, leading to cap thickening and increased plaque stability. Conversely, the removal of fibroblast-like cells during atherosclerosis progression results in reduced fibrous cap formation in mice receiving anti-IL-1β antibody treatment.
- Trevor P. Fidler
- Andrew Dunbar
- Alan R. Tall