Abstract :
[en] Type 1 diabetes (T1D) is a chronic disease resulting from the selective autoimmune
destruction of pancreatic islet ß cells. The absence and/or breakdown of immune selftolerance
to islet ß cells is now recognized as the essential cause for the development of the
diabetogenic autoimmune response. For a long time, a failure in peripheral tolerogenic
mechanisms was regarded as the main source of an inappropriate immune process directed
against insulin-secreting ß cells. While defective peripheral self-tolerance still deserves to
be further investigated, the demonstration that all members of the insulin gene family are
transcribed in thymic epithelial cells (TECs) of different species under the control of the
AutoImmune REgulator (AIRE) gene/protein has highlighted the importance of central self-tolerance to insulin-secreting islet b cells. Moreover, there is now evidence that a primary or acquired failure in thymus-dependent central self-tolerance to ß cells plays a primary role in T1D pathogenesis. This novel knowledge is currently translated into the development of
innovative tolerogenic/regulatory approaches designed to reprogram the specific immune
self-tolerance to islet ß cells.
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