Atherosclerosis has been widely recognized as a slow progressing inflammatory disease of the arterial
walls involving both inflammation and autoimmune processes with a complex etiology in which the immune system
plays a key role. A hallmark of atherosclerosis is that the macrophages pick up the lipids to form the foam cells
which build up the plaque in the arterial wall. Consequently, the arteries become narrowed.
Plaque rupture can trigger thrombosis which is superimposed on atherosclerotic lesion. The activation of macrophages
and T cells plays key roles in these lesions. Cells involved in the atherosclerotic process secrete soluble
factors, known as cytokines. These cytokines can be further divided into two classes namely proinflammatory and anti-inflammatory
cytokines based on their roles in inflammation. Among the cytokines, interleukin (IL)-35 is the one most recently discovered that
suppresses inflammatory responses of immune cells. Accumulating evidence suggests that IL-35 represents an attractive target for antiatherosclerotic
therapy based on its several atheroprotective features. In this review, we will provide a brief overview of IL-35 biology
and the role of IL-35 in the development, or the progression of atherosclerosis.