The article provides an overview of the immunology of type 1 diabetes (T1D), emphasizing the role of T cells. T1D is an autoimmune disease that leads to the destruction of pancreatic β-cells, requiring lifelong insulin treatment. The disease is triggered by a combination of genetic, environmental, and immunological factors. Genetic predisposition, particularly associated with human leucocyte antigen (HLA) genes, plays a significant role in T1D development. Environmental factors, such as viral infections and changes in the gut microbiome, also contribute to disease onset. Innate immune cells, including dendritic cells, macrophages, neutrophils, and natural killer (NK) cells, are involved in the early stages of T1D. Autoantibodies and B cells are important in disease pathogenesis, with B cells potentially acting as antigen-presenting cells. CD4+ and CD8+ T cells are key players in T1D, with specific clones targeting insulin and other autoantigens. The article discusses various therapeutic approaches, including targeting innate immune pathways, antigen-specific strategies, B cell-directed immunotherapy, costimulation blockade, and anti-thymocyte globulin. The recent approval of teplizumab, an immunotherapy targeting T cells, marks a significant advancement in T1D treatment. The article concludes by highlighting the need for further research to understand the mechanisms underlying T1D and to develop more effective treatments.The article provides an overview of the immunology of type 1 diabetes (T1D), emphasizing the role of T cells. T1D is an autoimmune disease that leads to the destruction of pancreatic β-cells, requiring lifelong insulin treatment. The disease is triggered by a combination of genetic, environmental, and immunological factors. Genetic predisposition, particularly associated with human leucocyte antigen (HLA) genes, plays a significant role in T1D development. Environmental factors, such as viral infections and changes in the gut microbiome, also contribute to disease onset. Innate immune cells, including dendritic cells, macrophages, neutrophils, and natural killer (NK) cells, are involved in the early stages of T1D. Autoantibodies and B cells are important in disease pathogenesis, with B cells potentially acting as antigen-presenting cells. CD4+ and CD8+ T cells are key players in T1D, with specific clones targeting insulin and other autoantigens. The article discusses various therapeutic approaches, including targeting innate immune pathways, antigen-specific strategies, B cell-directed immunotherapy, costimulation blockade, and anti-thymocyte globulin. The recent approval of teplizumab, an immunotherapy targeting T cells, marks a significant advancement in T1D treatment. The article concludes by highlighting the need for further research to understand the mechanisms underlying T1D and to develop more effective treatments.