Continued evaluation of such strategies, particularly in humanized models of the disease [124], should help to allay translational fears and facilitate the transit of DC-based therapies to patients. We apologize to our colleagues whose work could not be cited individually due to space restrictions. Relevant research by our group is supported by the National Institutes of Health, the Juvenile Diabetes Research Foundation International, the American Diabetes Association and the Irma T. Hirschl/Monique Weill-Caulier Trust. The authors declare no conflicts

of interest. “
“From many perspectives, cardiovascular high throughput screening diseases and cancers are fundamentally different. On the one hand, atherosclerosis is

a disease of lipid accumulation driven by diet and lifestyle, whereas cancer is an attack “from within” driven by mutations. Nevertheless, studies over the past 20 years have forced us to re-evaluate such a view. We are learning that, among other factors, the immune system is indispensable for the development and progression of both diseases. Its components are not only reactive but can also orchestrate both tumor and atherosclerotic lesion growth. In this Viewpoint, we explore how monocytes, which are key constituents of the immune system, forge links between cardiovascular diseases and cancers. Cardiovascular diseases and cancers are the leading PLX4032 datasheet causes

of death worldwide. Collectively, they are responsible for nearly two thirds of all deaths in the United States and cost the global economy nearly 2 trillion dollars in direct and indirect costs each year 1, 2. It is now recognized that inflammation is a major contributor to how these diseases arise, develop and cause death. A groundbreaking paper in 1998 by Charo and co-workers 3, for example, demonstrated that deletion of CCR2, a chemokine known to drive the accumulation of inflammatory monocytes in atheromata, attenuates atherosclerosis. More recently, Pollard and co-workers Baf-A1 molecular weight 4 demonstrated that CCR2 controls the accumulation of inflammatory monocytes in breast cancer metastases and enhances cancer progression. These studies illustrate how a common feature, in this case the chemokine receptor-dependent accumulation of a particular monocyte subset, can influence the course of both diseases. Monocytes are circulating cells that can be separated into at least two functionally distinct subsets. The heterogeneity suggests that subsets are predestined in the blood for particular phenotypes in tissue. Recent research has focused mostly on inflammatory or classical Ly6Chigh CCR2high monocytes, because these cells selectively expand in experimental models of atherosclerosis and cancer and drive disease progression.