Figure 1.

DM pathogenesis. DM is an immune-modulated disease. For T1DM, antigen presentation by B cells and DCs drives the activation of β−cell-specific T cells. In addition, the exposure of B cells to β−cell autoantigens leads to the production of islet β−cell targeting autoantibodies. These lead to β−cell destruction. For T2DM, IFN-γ production by activated CD4⁺ T cells activates macrophages to produce IL-1β and TNF. This low chronic-grade inflammation causes insulin resistance or inhibits insulin uptake in tissues. In addition, the cytokines cause insulin secretion by β-islet cells to compensate for reduced insulin sensitivity. These stimulate the Islet β cells to produce insulin. Persistent IL-1β and TNF production triggers β-cell islet destruction.