Autoimmunity is a condition in which the body produces an immune response directed against its own tissues. It is essential that the body be able to recognize "self" from "non-self" for survival. Normally, individuals do not form destructive antibodies to themselves, only to foreign material (antigens). This is because the body has developed a tolerance to the antigens normally present within self. This state of immune tolerance to self antigens is maintained by a complex network of T and B lymphocytes and their regulatory products. However, in certain diseases, one can produce antibodies to one's own cells or tissue components. This type of antibody is called an auto-antibody and diseases associated with these antibodies are called autoimmune diseases. Very modest degrees of autoimmune reactivity against self-antigens or self-antibodies can occur and are normal. However, the appearance of normal auto-antibodies must be a carefully controlled event. If, for example, lymphocytes proliferate and large quantities of auto-antibodies are produced, attack of self and autoimmune disease can occur.

Several conditions must be in place before an autoimmune process can occur. The first is a genetic susceptibility for the host immune system to misinterpret foreign antigens in the environment and to recognize self as foreign, as the result of that misinterpretation. Second, the host must be exposed to the foreign antigen that triggered the cascade. Finally, the intact foreign antigen must be presented to the mucosal immune system following its paracellular passage (normally prevented by tight junction competency) into the body. Studies have suggested that increased intestinal permeability is involved in the pathogenesis of various autoimmune diseases and is key to the presentation of antigen to submucosa.

In many cases, increased intestinal permeability appears to precede disease and causes an abnormality in antigen delivery that triggers the processes leading to the autoimmune response. Recent studies have linked the presence of increased intestinal permeability to the occurrence of clinically evident celiac disease, type 1 diabetes, primary biliary cirrhosis, autoimmune hepatitis and systemic sclerosis.