Lee Tucker

TL;DR: T cells from prediabetic NOD mice respond spontaneously to these peptide analogs in culture; this finding validates them as being related to a critical autoantigen involved in the etiology of spontaneous diabetes and indicates that their further characterization is important for a better understanding of underlying disease mechanisms.

TL;DR: It is now clear that the major function of NKT cells in the immune system is not related to their interleukin (IL)-4 secretion and, activated in the presence of IL-12, acquire a strong inflammatory phenotype and cytotoxic function.

TL;DR: It is shown, by adoptive transfers, that prediabetic or diabetic NOD splenocytes upon encountering IL-10 in the pancreatic islets readily promoted diabetes, suggesting that the compartment of exposure, not the timing, confers proinflammatory effects on this molecule.

TL;DR: The mechanisms underlying IL-4-mediated activation of the self-reactive BDC2.5 T cells could have triggered self-antigen presentation within the pancreatic islets both by driving maturation of DC from a tolerizing to a priming state and by increasing self-Antigen uptake by macrophages.