Pathogenesis of type I DM.

chronic autoimmune attack on β cells

manifestations of the disease (hyperglycemia and ketosis) occur late in its course, after more than 90% of the β cells have been destroyed

T lymphocytes react against β-cell antigens and cause cell damage: include CD4+ TH1 subset, which activates macrophages, and CD8+ cytotoxic T lymphocytes, which directly kill β cells

cellular necrosis and lymphocytic infiltration. This lesion is called insulitis

IFN-γ, produced by T cells, and tumor necrosis factor and interleukin-1

Autoantibodies against a variety of β-cell antigens, including insulin and glutamic acid decarboxylase( GAD) can be found

Associated with HLA-DR3, or DR4 type of MHC II antigens

some viral antigens are antigenically similar to β cell antigens (molecular minicry),