New therapeutic approaches for type 1 diabetes: Disease-modifying therapies

Figure 1 Immunopathogenesis of type 1 diabetes mellitus. Autoantigens from pancreatic islet β-cells are presented by antigen-presenting cells (APCs), thereby activating T cells including helper T (Th) cells type 1 and type 17 and cytotoxic T lymphocytes (CTLs). Th type 1 cells play a key role in the development of the autoimmune response. They stimulate the activity of inflammatory T cells, macrophages and natural killer (NK) cells by producing proinflammatory cytokines and stimulate B cells (B), which produces autoantibodies and inhibits the protective Th type 2 cell function. Together, these immune cells contribute to the destruction of pancreatic β-cells. Red line: Inhibition; Green line: Stimulation. GADA: Glutamic-acid-decarboxylase antibody; IA2: Islet tyrosine phosphatase 2 antibody; IAA: Insulin autoantibody; ICA: Islet cell antibody; IL: Interleukin; IFN-γ: Interferon γ; TGF-β: Transforming growth factor β; TNF-α: Tumor necrosis factor α; Treg: Regulatory T cell; ZnT8: Zinc transporter 8 antibody.