Atherosclerosis, the buildup of fatty plaques in blood vessel walls, is a major cause of human mortality. Chronic inflammation and elevated levels of CCL17 have been linked to the progression of atherosclerosis. Researchers have uncovered a new signaling pathway involving CCR8, shedding light on the role of CCL17 in cardiovascular disease. This pathway suppresses anti-inflammatory regulatory T cells, driving atherosclerosis. Understanding these interactions is crucial for developing targeted interventions that minimize pathology without compromising necessary immune system activity.
The signaling protein CCL17, produced by dendritic cells, influences the activity and mobility of T cells. Elevated CCL17 levels are associated with increased risk of atherosclerosis and inflammatory cardiovascular and digestive diseases. In a recent study, researchers demonstrated that CCL17 signals through an alternate receptor, CCR8, triggering a signaling pathway that suppresses anti-inflammatory Treg cells and drives atherosclerosis. Genetic ablation of CCL3 and CCR8 in T cells reduced atherosclerosis, highlighting the potential of targeting this pathway for intervention. These findings provide valuable insight into the role of CCL17 in cardiovascular disease and the potential for targeted interventions to reduce inflammation and combat atherosclerosis.
