Rheumatoid Arthritis is a serious, debilitating disease that causes pain and permanent damage to the joints. 
The small joints of the hands, feet, wrists, and ankles are most often affected, but disease can occur in shoulders, knees and hips as well. Rheumatoid Arthritis affects over 3 million adults in the US and is three times more common in women than men. Once diagnosed, patients with Rheumatoid Arthritis need to take powerful immune-suppressing drugs for the rest of their life.
The clinical challenge of Rheumatoid Arthritis is that despite treatment, disease signs re-surface in many patients, sometimes as often as every few years. 
It is during these disease relapses or “flares” that debilitating pain and irreversible tissue damage to the joints occurs. The reason that relapse flares happen in Rheumatoid Arthritis is thought to relate to the complex etiology of the disease, which involves two distinct cellular mechanisms.
The first cellular mechanism of Rheumatoid Arthritis is a systemic auto-immune reaction to as-yet-unidentified antigens that causes chronic inflammation within the joints. In turn, this triggers a second cellular mechanism characterized by uncontrolled growth of the synovial membrane that lines the joint space, which forms a tissue mass that invades the joint and ultimately destroys it.
Available treatments for Rheumatoid Arthritis target the first disease mechanism by suppressing the body’s immune system. 
The disadvantage of relying on treatments targeting only one disease mechanism is that few options remain for patients when they experience painful relapse flares, other than increasing their drug dose, which can cause dangerous side-effects, or switching to another closely-related treatment, which is not always successful.
A treatment for Rheumatoid Arthritis that targets the second disease mechanism by suppressing uncontrolled growth of the joint synovial membrane cells might be useful as an adjunct therapy to better control refractory disease. The goal of our research is better understand the changes that occur in the synovium of the joints of Rheumatoid Arthritis patients, and to use this information to develop a new disease treatment that targets the synovial membrane overgrowth that is responsible for joint pain and destruction.
We are studying a naturally-produced 
protein that suppresses cellular growth. We are investigating the effects of this protein on synovial fibroblasts from Rheumatoid Arthritis patients. We are also using a mouse model to test the effects of the protein against Rheumatoid Arthritis disease signs. By better understanding the protein’s natural function, we hope to one day develop a therapy that is both effective and safe.
Caroline Dealy, PhD. 