JCI table of contents: January 2, 2007

TITLE: Chronic lymphocytic leukemia requires BCL2 to sequester prodeath BIM, explaining sensitivity to BCL2 antagonist ABT-737

AUTHOR CONTACT:

Anthony Letai,
Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
Phone: (617)-632-2348; Fax: (617)-582-8160; E-mail: .
View the PDF of this article at: https://www.the-jci.org/article.php?id=28281

CARDIOVASCULAR BIOLOGY

Complex macrophage and monocyte interactions at work in atherosclerosis

Monocytes and macrophages are prominent cell types involved in the body's response to the development of atherosclerotic plaques – a build-up of cholesterol and fatty material within arteries due to the effects of the inflammatory condition atherosclerosis. Three independent studies appearing in the January issue of the Journal of Clinical Investigation provide evidence in animal models of genetic- and high-fat diet–induced disease that: (i) distinct subsets of monocytes give rise to the macrophages present in atherosclerotic plaques; (ii) there is differential expression of chemokine receptors on the surface of these cell subsets; and (iii) consumption of a high-fat diet causes a subset of macrophages not normally present in fatty tissue under normal dietary conditions to travel there and to behave differently.

In the first study, Mikael Pittet and colleagues from Massachusetts General Hospital demonstrate that a subset of monocytes that express a high level of a marker antigen, Ly-6C, give rise to macrophages present in atherosclerotic plaques. In the second related study, Gwendalyn Randolph and colleagues from Mount Sinai School of Medicine in New York show that monocyte subsets differentially expresses the chemokine receptors CCR2, CCR5, and CX3CR1 in order to enter atherosclerotic plaques. In the third of this trio of articles, Alan Saltiel and colleagues from the University of Michigan document that macrophages from fatty tissue, which accumulate during obesity and are implicated in the development of insulin resistance and diabetes, undergo phenotypic changes to become proinflammatory.