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T cell regulatory circuitry: antigen-specific and TCR-idiopeptide-specific T cell interactions in EAE.

The presence of self-reactive T cells and self-recognition is now considered important for the normal functioning of the immune system. The demonstration of the involvement of self-MHC and bound self-peptides in the thymus for both positive as well as negative selection during T cell development clearly established a key role for recognition of the self [I]. Although many autoreactive T cells are deleted in the thymus, others are not purged and survive in the periphery. It has been estimated that the mouse genome could encode for at least 50,000 different proteins. If the immune system were to delete self-reactive T cells to all possible determinants on all self-proteins, it would very likely compromise defensive readiness. Granting the presence of a large cadre of self-reactive cells, directed against selfantigens, it is essential to consider how the inevitable bouts of self-reactivity can be controlled [2]. In this review we will be primarily discussing our work on the induction of the murine autoimmune disorder, experimental allergic encephalomyelitis (EAE), and its regulation. We will also focus on attempting to formulate a cogent regulatory circuitry that could correlate antigenic induction with eventual TCR-idiopeptide-based regulation.