Rheumatoid Arthritis and The Role of a Single Monocyte

An estimated 1.3 million people in the United States suffer from rheumatoid arthritis. The causes behind this chronic disease — which can exhibit itself as pain, swelling, stiffness, deformation, and loss of function in the joints — have eluded scientists for centuries. A new study by UNC researchers offers tantalizing glimmers about the roles of a gene called CCR2, an immune system cell called Th17 cell, and a missing monocyte.The study contributes to a better understanding of the disease mechanism and has implications to guide the clinical trial strategy, said lead researcher Peng Liu, MD, PhD, research assistant professor at the UNC Thurston Arthritis Research Center. Her team's findings were reported online in PLoS One on Oct. 4.The mystery began several years ago when arthritis researchers zeroed in on a gene called CCR2. CCR2 is highly expressed in the joints of patients with rheumatoid arthritis, which led researchers to believe it might contribute to the disease. "Scientists thought that if you inhibited CCR2 you would have a beneficial effect," said Liu. "But actually, the result was the opposite." Studies revealed that suppressing CCR2 in fact cannot ameliorate joint inflammation, in some cases, it leads to disease exacerbation.
Intrigued, Liu and her team used mice to investigate how CCR2 affects immune system cells. The immune system is critical because rheumatoid arthritis is an autoimmune disease, in which the immune system attacks the body's own tissues, causing inflammation.