Rheumatoid Arthritis Investigation

Autoimmune diseases are very interesting to study because of the mechanisms that underlie their existence and how the body mistakenly begins to fight itself. I chose to investigate the autoimmune disease Rheumatoid arthritis because my father has been diagnosed with Arthritis and I was interested in becoming knowledgeable of what could possibly be going on the inside of my father’s body.

            Rheumatoid Arthritis (RA) is an autoimmune disease in which our immune system attacks its own joints, resulting in inflammation on the inside (synovium) and bone deterioration. As the synovium thickens this tends to cause swelling and pain which usually leads to a loss of mobility. The joints at risk for RA include the hands, feet, wrists, elbows, knees and ankles. Interestingly this disease usually affects joints symmetrically, meaning that if one elbow becomes impaired it is very likely that the other elbow will be affected as well. The etiology of RA is currently uncertain but research has been able to detect many of the important immune components that trigger the inflammation and bone resorption.

            Some of the chemical mediators that trigger inflammation in RA include kinins and vasoactive amines. Kinins are a group of polypeptides that have the ability to stimulate smooth muscle, increase vascular permeability, induce pain and possibly promote leukotaxis. Histamine, a vasoactive amine is believed to have a major role in the initiation of the inflammatory response in RA. It also encourages vasodilation and vascular permeability. Lysosomes which are involved in the digestive and lytic process of cells have been suggested to release their enzymes directly into cell cytoplasm or surrounding tissue in RA, which injures the tissue and triggers the inflammation response. If this action is prolonged it results in the continuous production of autoantibodies because of the antigenic stimulation by degraded host tissues.

            Patients with RA have an increased number of T cells, which is explained by the role they play in triggering osteoclastogenesis. Osteoclstogenesis is the development of osteoclasts, which are bone cells that are specialized to reabsorb calcified tissue. This is the reason why patients with rheumatoid arthritis experience the pain they do, because with time their bones start to become fragile due to the action of these overstimulated osteoclasts. T cells express RANKL which is a member of the TNF family of cytokines. RANKL induces osteocalstogensis from monocytes or macrophages.  

 

Wilder, Ronald L. "Immunopathogenesis of Rheumatoid Arthritis." Clinical Immunology Newsletter 6.1 (1985): 1-5. Web

Panayi, G. S. "Developments in the Immunology of Rheumatoid Arthritis, a Personal Perspective." Rheumatology 50.5 (2011): 815-17. Web.