The role of innate and adaptive immunity systems and induction in T1DM patients. The initiation T1D takes place in the pancreas, when dendritic cells (DCs) and macrophages uptake and present β-cell antigens to T-cells to activate CD4+ and CD8+ T-cells. Then, activated CD4+ and CD8+ T-cells lead to the damage of β-cells. At the same time, DCs, macrophages, neutrophils, and NK cells as well as damaged β-cells can produce a large number of proinflammatory cytokines such as TNF-α and IFN-γ, which can directly contribute to β-cells’ death. And these immune cells interact with each other to enhance their activation state. B-cells present β-cell antigens to diabetogenic T-cells and release autoantibodies to damage β-cells. iNKT cells can promote the recruitment of DCs. Mast cells facilitate the differentiation of Th17 by producing IL-6, and this effect can be inhibited by Tregs. The crosstalk between innate and adaptive immune cells contributes to the progression or prevention (not shown) of T1D.