Autoimmune diseases are a family of illnesses with the common pathogenesis of an immune system-mediated attack on the body’s own organs. The mechanisms for the development of autoimmune disease are related to failure to distinguish self from nonself. In patients with autoimmune disease, B cells, T cells and antibodies are present which recognize antigens and are reactive to antigens in the body of the host. Disorders referred to as “autoinflammatory responses” are a group of human diseases that share many of the same inflammatory mediators but lack evidence of self-reactive lymphocytes. These disorders usually have a genetic component and evidence of innate immune system activation. Autoimmune diseases progress gradually and can result in serious tissue damage before clinically diagnosed.
The majority of autoimmune diseases have multiple underlying genetic factors. Both genetic predisposition and environmental factors are thought to both play a role in autoimmune diseases. Predisposition to autoimmunity may be influenced by the microflora, bacteria that live in and on the body.
Autoimmune thyroid disease (autoimmune thyroiditis) and type I diabetes are the most common autoimmune diseases. Some autoimmune diseases are organ specific such as primary biliary cirrhosis and others involve multiple organs such as lupus erythematosus (SLE).
Therapeutic approaches to treat autoimmune disease include the use of biological agents that modify specific inflammatory and/or effector pathways. Treatments aim to modify the host immune system to restore tolerance. Immunotherapies that suppress the immune system are used to dampen autoimmunity, treat allergies and reduce organ transplant rejection. Regulatory T cells (Tregs) and engineered Tregs are used or in development as immunotherapies to treat autoimmune disease and inflammatory conditions such as type 1 diabetes, rheumatoid arthritis, inflammatory bowel disease and graft-versus-host disease.