| Abstract | Recent experimental observations have revealed that during the onset of autoimmune Type 1 Diabetes (T1D), different clones of T cells with various T cell avidities and protein specificities are naturally generated in diabetic animal models. One particular protein IGRP, the most dominant autoantigen, is responsible for activating low and high avidity IGRP-specific T cells via APCs. Although high avidity T cells destroy ~90% of beta cell repertoire, leading to the abolishment of insulin secretion crucial for glucose metabolism, low avidity T cells appear to play a protective role. Several hypotheses concerning the kinetics of these low avidity T cells and the effects of certain drug treatments on this populations have been suggested. We present here series of mathematical models that investigate these hypotheses and the outcome of certain drug treatments. We also examine the various features exhibited by the T cell clones. |
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