Autoimmune diseases involve the development of antibody or cell-mediated immune responses directed against self antigens ( 88,92). In many autoimmune diseases, an individual's risk is affected by his or her HLA genes (2,3 and 4,93,94). There are several possible scenarios under which such undesirable responses might be initiated.

Autoimmune responses may arise when antigens that have been normally sequestered from the immune system (e.g., in immunologically privileged sites) are exposed as a result of trauma. Having never been detected previously by the immune system as it developed its sense of self versus nonself, such antigens are now seen as foreign. Second, the interaction of self molecules with small reactive chemicals (e.g., haptens) or with infectious agents may produce alterations in self molecules (altered antigens or neoantigens), resulting in their detection as nonself. Third, immune responses against determinants on infectious agents may generate clones of lymphocytes with receptors capable of cross-reacting with self antigens (cross-reactive antigens). A classic example is rheumatic fever, which results from immune responses against streptococcal antigens that are cross-reactive with molecules found on cardiac tissue. Finally, some autoimmune responses, especially those that tend to develop in later life, may result from senescence of inhibitory mechanisms, such as suppressor T lymphocytes, that keep autoimmune responses under control. For example, the onset of systemic lupus erythematosus is associated with age and an accompanying decline in suppressor T-cell function.

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