Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of pancreatic β-cells by the immune system, leading to insulin deficiency. Recent advances in immunotherapy, such as the approval of a T-cell-targeting treatment, highlight the critical role of the immune system in T1D pathogenesis. Understanding the immunology of T1D is essential for developing effective interventions. This review summarizes the immune mechanisms underlying T1D, focusing on T cells, and discusses the genetic, environmental, and immunological factors that contribute to its development. Genetic factors, including HLA alleles and other genes, play a significant role in T1D susceptibility. Environmental factors, such as viral infections and the microbiome, are also implicated in disease progression. Innate immune cells, including dendritic cells, macrophages, neutrophils, and NK cells, are involved in the early stages of T1D. Autoantibodies and B cells are important in disease pathogenesis, while autoreactive T cells, particularly CD4+ and CD8+ T cells, are central to the autoimmune attack on β-cells. The role of innate immunity, including cytokines like IL-1 and type 1 interferons, is also discussed. Therapeutic strategies targeting immune pathways, such as costimulation blockade, B-cell depletion, and T-cell modulation, are explored. The approval of teplizumab, an immunotherapy that delays or prevents T1D progression, marks a significant milestone in T1D treatment. Future directions include the development of combination therapies and the application of advanced imaging techniques to better understand immune cell populations in T1D. The review emphasizes the importance of understanding the complex interplay between genetic, environmental, and immunological factors in T1D and the need for targeted, personalized approaches to treatment.Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of pancreatic β-cells by the immune system, leading to insulin deficiency. Recent advances in immunotherapy, such as the approval of a T-cell-targeting treatment, highlight the critical role of the immune system in T1D pathogenesis. Understanding the immunology of T1D is essential for developing effective interventions. This review summarizes the immune mechanisms underlying T1D, focusing on T cells, and discusses the genetic, environmental, and immunological factors that contribute to its development. Genetic factors, including HLA alleles and other genes, play a significant role in T1D susceptibility. Environmental factors, such as viral infections and the microbiome, are also implicated in disease progression. Innate immune cells, including dendritic cells, macrophages, neutrophils, and NK cells, are involved in the early stages of T1D. Autoantibodies and B cells are important in disease pathogenesis, while autoreactive T cells, particularly CD4+ and CD8+ T cells, are central to the autoimmune attack on β-cells. The role of innate immunity, including cytokines like IL-1 and type 1 interferons, is also discussed. Therapeutic strategies targeting immune pathways, such as costimulation blockade, B-cell depletion, and T-cell modulation, are explored. The approval of teplizumab, an immunotherapy that delays or prevents T1D progression, marks a significant milestone in T1D treatment. Future directions include the development of combination therapies and the application of advanced imaging techniques to better understand immune cell populations in T1D. The review emphasizes the importance of understanding the complex interplay between genetic, environmental, and immunological factors in T1D and the need for targeted, personalized approaches to treatment.