Abstract
Abstract
Atherosclerosis is a chronic inflammatory disease of the arterial wall responsible for most ischaemic cardiovascular diseases. Both innate and adaptive immune responses have been involved in the initiation and progression of atherosclerosis. However, there is currently no specific therapeutic strategy targeting the immuno-inflammatory response in this disease. Deciphering the role of specific subtypes of immune cells would lead to new, potent and specific therapeutic strategies to limit these devastating diseases.
We have shown that subpopulations of regulatory T (Treg) cells potently inhibit atherosclerotic lesion development and inflammation. More recently, we have shown that loss of suppressor of cytokine signaling (SOCS)3 in T cells increases both interleukin (IL)-17 and IL-10 production, induces an antiinflammatory macrophage phenotype, and leads to unexpected IL-17–dependent reduction in lesion development and vascular inflammation. These results identify novel SOCS3-controlled IL-17 regulatory pathways in atherosclerosis and may have important implications for the understanding of the increased susceptibility to vascular inflammation in patients with dominant-negative STAT3 mutations and defective Th17 cell differentiation.