To get this semester's blogging off and running (no one wants to be the first to post on an empty blog!), here is my take on a new PNAS paper from the Cantor lab:
Rheumatoid arthritis (RA) is an autoimmune inflammatory disease that affects around 1.3 million people in the United States. Found more commonly in women than men, this disease causes pain and swelling in the joints, and can lead to cartilage and bone loss, and joint deformity. RA is commonly treated with methotrexate, in combination with other drugs, but treatments can be expensive, with lifetime direct costs of up to $180,000 per patient (in 2010 dollars). These treatments can also have adverse side effects. The prevalence of RA in the U.S. is increasing as the population ages, suggesting a need for continued research into the causes of, and potential new therapeutics for, RA.
At its core, RA is a disease of multiple immune cell types. One component is B cells, which produce antibodies that recognize “self” proteins found in connective tissue. A second component is “helper” T cells (also termed CD4 T cells), which help B cells produce antibody, and which contribute to an inflammatory state in the joints. A study published this week in the Proceedings of the National Academy of Sciences by Leavenworth and colleagues further refines the contribution of different CD4 T cell subsets in RA, and defines a new role for yet a third cell type, natural killer (NK) cells, in suppressing the development of RA. To do this, the authors used an experimental mouse model of RA, induced by injection of type II collagen, a prominent component of connective tissue, under the skin. This model (collagen-induced arthritis; CIA) causes many of the same symptoms as human RA, and has been used to test a number of new treatments for RA (1).