Juntang Lin, Vijay Kakkar and Xinjie Lu Pages 5151 - 5159 ( 9 )
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.
IL-35, atherosclerosis, regulation t cell, knock out mice and cytokine.
Mary and Garry Weston Molecular Immunology Laboratory, Thrombosis Research Institute, London, SW3 6LR, United Kingdom.