**4. Conclusion**

In ADs, the immune system recognizes and attacks its tissues i.e., self-destruction. Activation, proliferation, and apoptosis of immune cells are dependent on the controlled production of ROS. However, under chronic inflammatory conditions, large amounts of ROS generated are responsible for the pathophysiology of many human disorders. A characteristic feature of ADs is the presence of autoantibodies and inflammatory conditions and cells such as mononuclear phagocytic system, autoreactive T lymphocytes and autoantibody-producing B cells (plasma cells). RA is a systemic autoimmune disease of the joints with underlying synovitis and is also known as inflammatory arthritis. Increased apoptosis and decreased clearance of apoptotic cells observed in systemic autoimmunity may be a be contributing factors in autoimmune disorders such as RA and SLE. Since ROS have been implicated in the initiation and progression of autoimmunity, their role in autoimmunity remains complex. The pathophysiology of ROS in RA though not well understood but could be understood as an imbalance in homeostasis between pro- and antioxidant conditions and pro and anti-inflammatory states, which may become chronic leading to led to damage of connective tissue and multiple joints and other organs in the body. Moreover, it is important to consider the therapeutic development of antioxidants and selective ROS inhibitors as a tool that could be used in the prevention and treatment of a broad range of ADs.
