Conclusions

The clinical syndromes of AITD are well established. The pathogenetic mechanisms are now also increasingly well understood. Recombinant DNA technology has provided the necessary tool for the elucidation and characterization of the target auto-antigens. Establishment of B cell epitopes and, through cloning of target tissue T cells, the definition of T cell epitopes, will almost certainly tie up the pathogenesis story. Two issues remain: what is the etiology and in this context what does the environment contribute, and can we modulate or prevent AITD?

Cloning of the autoantigens will allow an answer to the first question through approaches such as examination of homologies between these autoantigens and infectious agents. The second question is more difficult. With the understanding we now have and the strategies available there seems little reason, once the relevant autoantigenic epitopes are established, why prospects for autoimmune disease should be any different from those of infectious diseases and why immunization against AITD should not become a reality. Studies in animal models of AITD using oral tolerance as a therapeutic option also offer an exciting alternative strategy.

See also: Autoantibodies, tests for; Autoantigens; Autoimmune disease, pathogenesis; Autoimmune disease, spontaneous animal models; Autoimmune diseases; Autoimmunity; Eye, autoimmune disease; Molecular mimicry; Polyendocrine autoimmunity; Thyroid autoimmunity, animal models.

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