The ACR/ARHP Annual Scientific Meeting is the premier event for specialists in the field of rheumatology. At this year’s meeting, basic researchers will have multiple opportunities to increase their knowledge, and there will be something for every interest.
There are several exciting offerings planned for basic researchers, but they aren’t the only attendees who can benefit from basic science sessions—clinicians can attend these talks to obtain important information from the bench that will directly help them when they return to the bedside.
“There will be many wonderful basic science talks at the ACR’s annual meeting in Atlanta,” explains ACR Annual Meeting Planning Committee Member R. John Looney, MD. “As an academic clinician and someone involved in clinical trials, I will be particularly interested in talks that provide insight into the pathogenesis of autoimmune diseases and their complications. I have always been fascinated by these talks. As a bonus, they have proven to be an excellent source of ideas for new therapies.”
Here are a few basic science sessions the planning committee has identified as being of interest to both basic researchers and clinicians.
Innate Immunity
Innate immunity plays a key role in inflammatory diseases such as gout and pseudogout and can play a role in chronic autoimmune inflammation and inflammation induced by damage or injury. The molecular details of signals used in innate immunity are now being realized, raising the possibility of new therapeutic interventions. To get the latest updates on innate immunity, be sure to add these three sessions to your annual meeting itinerary:
- ACR Immunology Updates for Clinicians: Innate Immunity and Inflammation (Monday, November 8; 9:00–10:00 am)
- ACR Basic Science Symposium: Toll-like Receptors and Inflammation: Towards Innovative Treatment of Rheumatoid Arthritis (Monday, November 8; 2:30–4:00 pm)
- ACR Basic Science Symposium: Cell Death: Receptors, Sensors, and Inflammatory Pathways (Wednesday, November 10; 2:30–4:00 pm)
Macrophages
Macrophages are ubiquitous and extremely adaptable. They can become Kupffer cells, type A synoviocytes, alveolar macrophages, or osteoclasts. They can clear debris, kill microorganisms, and enhance wound healing—or, they can cause chronic inflammation, fibrosis, osteolysis, and atherosclerosis. Understandably, regulating macrophage differentiation and activation has become a hot topic in rheumatology. If you are interested in macrophages, don’t miss the following sessions:
- ACR Immunology Updates for the Clinicians: Macrophage Differentiation (Tuesday, November 9; 7:15–8:15 am)
- ACR Basic Science Symposium: A Critical Role for Lipid Metabolism in the Interplay Between Atherosclerosis and Autoimmune Disorders (Wednesday, November 10; 4:30–6:00 pm)
Epigenetics
Epigenetics—the alteration of mesencymal cells to a more inflammatory and/or profibrotic phenotype—is one of the great challenges of chronic inflammation. Although there has been debate, this transformation appears to be due to heritable, nonmutational changes in gene regulation (i.e., epigenetic changes). Similarly, epigenetic changes in gene expression induced by DNA methylation inhibitors such as hydralazine or procainamide may be responsible for certain types of drug-induced lupus. These days, epigentics seems to be a growing topic of discussion, and below are two sessions that address this topic:
