Rheumatoid arthritis (RA) and the Immune System

Rheumatoid Arthritis and Normal JointRheumatoid arthritis (RA) is an autoimmune disorder that causes severe disability and loss of quality of life. Women are two to three time more likely to be diagnosed with rheumatoid arthritis than men.

The disease is characterized by inflammation in joints, swelling, formation of self-reacting antibody proteins, and cartilage and bone loss throughout the body. Morning stiffness and fatigue are also common symptoms of the disease.  The thymus plays a critical role in the maturation of immune cells, such as type 1, type 2 and type 17 helper T cells.

While the cause of Rheumatoid arthritis is not fully understood, type 1 and type 17 helper T cells (Th1, and Th17) have been increasingly implicated as mediating the disease. Ordinarily, a critical T-cell homeostasis is maintained between pro-inflammatory T-cells (Type 17) and anti-inflammatory T-cells (Th1).

Both of these cells reach maturation in the thymus and produce a class of chemical messengers known as interleukins to affect their regulatory functions. It is thought that environmental and genetic factors cause Th17 over-production, which shifts the T-cell population away from Th1 maturation and toward inflammation. Imbalance between T-cell homeostasis is thought to be a significant cause of Rheumatoid arthritis.

Additionally, a host of other cell-types produced within the thymus play a critical role in mediating the downstream effects of Rheumatoid arthritis; these include macrophages, neutrophils and mast cells interacting with osteoclast and osteoblast to affect bone remodeling. Once inflammation is triggered, these cells migrate into joints and draw extra fluid with them into joints. This causes synovitis, swelling in the joints. Targeting each of these cells and the chemicals they secrete are strategies underway to reduce the incidence and severity of living with rheumatoid arthritis.

One of the challenges of aging is that the thymus gland shrinks and eventually does not produce the necessary thymic protein needed to mature the T-cells needed to mediate the proper immune responses. This could be a reason that RA advances with age. More recent studies link the chronic inflammatory process to diet and inflammation producing foods like gluten and sugar.