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Molecular Mimicry and Determinant Spreading, Page 1 of 2
< Previous page Next page > /docserver/preview/fulltext/10.1128/9781555818074/9781555811945_Chap15-1.gif /docserver/preview/fulltext/10.1128/9781555818074/9781555811945_Chap15-2.gifAbstract:
One of the most intensively studied animal models of autoimmunity is insulin-dependent diabetes mellitus (IDDM) in the nonobese diabetic (NOD) mouse. This chapter considers how molecular mimicry, when viewed in the broader context of degeneracy of T-cell recognition specificity, provides a rationale for the existence of frequent autoimmunity. Whether the initiating event is a viral infection or inflammation at a site where APCs become ready to present and process self-antigens or foreign antigens efficiently, the commonality is the presentation of unusual, generally nondisplayed antigenic determinants to T cells which have evaded the mechanisms of self-tolerance induction. For autoimmunity to occur, it is absolutely necessary for the initiating response to expand. Accordingly, since so many T cells potentially can be addressed by a large diversity of ligands, it is clear that many, apparently redundant regulatory mechanisms must have evolved to ensure the sanctity of the self from errant breakaway clones. In the first decades of the 21st century investigators will need to define and learn to mobilize and maintain these regulators.