Evidence suggests that some autoimmune diseases may result from superantigen stimulation of T cells. Superantigen involvement in turn implicates bacteria or viruses, since superantigens have usually been associated with microorganisms. It has been postulated that an imbalance in the composition of lymphocyte subsets may be responsible for autoimmunity, but no direct evidence for this mechanism exists for human autoimmune disease. Such dysregulation may include increased activity of suppressor T cells or imbalance between the T H1 and T H2 subsets of helper T cells. Exposure of protein antigens to lymphoid cells in the gut may induce peripheral tolerance that seems to prevent systemic immune responses to dietary proteins.
Oral tolerance is induced by at least two mechanisms.
One study shows that oral tolerance to myelin basic protein suppresses experimental autoimmune encephalomyelitis, a model for multiple sclerosis in humans. Results of these preliminary trials of orally induced tolerance have suggested possible benefits for this approach in multiple sclerosis and rheumatoid arthritis. The process is initiated by one of several ligand-receptor interactions and proceeds through activation of endonucleases as a consequence of the generation of intracellular messengers. Apoptosis can also be initiated by the absence of growth factors such as IL-2. Of possible importance in autoimmune disease is the Fas-Fas ligand system.