Fig. 1.

Development of autoimmune diabetes in the non-obese diabetic (NOD) mouse. At around 2 weeks of age a wave of apoptosis occurs among the pancreatic β-cells of the islets of Langerhans, as a part of natural pancreatic development (a). This leads to the presentation of β-cell derived antigens on dendritic cells in the pancreatic lymph nodes and activation of β-cell specific T lymphocytes (b). From 3 to 4 weeks of age lymphoid cells start to infiltrate the pancreas (c), initially as a non-invasive peri-islet infiltrate (d). With time the benign infiltrate develops into an aggressive state, in which T lymphocytes enter into the islet and destroy β-cells (e). When less than 10% of the β-cell mass remains, starting to occur at 10–12 weeks of age (f), blood glucose levels can no longer be maintained and the mice become diabetic. At 25–30 weeks of age around 80% of female NOD mice have developed disease (g), while only 20–30% of the male mice are affected.