Uncovering clues about a subtype of immune cells that contributes to heart disease

Role of IRF5 in the function of CD11c+ macrophages in atherosclerosis

Obesity and type 2 diabetes are ‘metabolic’ diseases that increase the risk of atherosclerosis, a build-up of fatty material inside the arteries. When these fatty plaques break apart they can trigger a heart attack or stroke. A common feature of metabolic diseases is the activation of a type of immune cells called macrophages. Professor Claudia Monaco and her team are studying the role of macrophages in atherosclerosis that happens as a result of metabolic diseases. They have identified a molecule called IRF5 that acts as a “switch”, turning on a certain type of macrophages called CD11c+. They also showed that obese mice lacking IRF5 have fewer CD11c+ macrophages and lower levels of atherosclerosis in their blood vessels. In this study, Professor Monaco and her team want to further explore the detailed biology of CD11c+ macrophages and how they contribute to atherosclerosis and plaque rupture. Understanding exactly how IRF5 leads to the activation of these damaging macrophages could reveal new ways to target and disrupt them. Medicines that prevent the harmful actions of CD11c+ cells may one day be an important weapon in the fight against atherosclerosis and heart attacks in people with metabolic diseases like type 2 diabetes.