ATLANTA—Rheumatologists are well aware that patients with rheumatoid arthritis (RA) and other chronic inflammatory disorders are at an increased risk of developing cardiovascular disease. It has also been established that high-density lipoprotein (HDL) levels correlate inversely with cardiovascular risk. Recent research, such as the study by Carpintero et al, which was led by a team of Swiss, Italian, and Australian investigators, have begun to narrow in on HDL’s ability to interfere with T-cell binding to monocytes, inhibiting production of proinflammatory cytokines.1
These discoveries have led to an important question: Might the intersection of cholesterol metabolism, atherogenesis, and inflammatory signaling offer a potential pathway for interventional strategies to combat inflammatory disease? These were the questions addressed by the research scientists who presented at the session, “A Critical Role for Lipid Metabolism in the Interplay between Atherosclerosis and Autoimmune Disorders.” [Editor’s Note: This session was recorded and is available via ACR SessionSelect at www.rheumatology.org.]
Kerry-Anne Rye, PhD, a professor at the University of Sydney, Australia, addressed the question: “Is it possible to use HDL to attenuate arthritis?” She and her group have conducted experiments at the Heart Research Institute of Sydney, where she is associate director, aimed at exploring a possible use of HDL to counteract the inflammatory processes that result in joint erosion.
Dr. Rye prefaced her presentation of her group’s current work with a succinct description of HDLs. Although we commonly use one term to refer to high-density lipoproteins, she noted, they do not comprise a single entity. Rather, HDLs are a complex series of subpopulations of particles, all of which are continually being interconverted from one to another by a range of factors in the circulation. HDLs, she said, “start off as discoidal particles consisting of a phospholipid bilayer surrounded by apolipoproteins,” and are classified according to the presence of one or both of their main constituent apolipoproteins, apoA-1 and apoA-2.